MATCH Treatment Subprotocol V: Phase II Study of Sunitinib in Patients With Tumors With cKIT Mutations (Excluding GIST, Renal Cell Carcinoma or Pancreatic Neuorendocrine Tumor)
Phase: PHASE2
Conditions: Advanced Lymphoma, Advanced Malignant Solid Neoplasm, Refractory Lymphoma, Refractory Malignant Solid Neoplasm, Refractory Multiple Myeloma
Sponsor: National Cancer Institute (NCI)

i
28 State Street, Suite 1100, Boston, MA 02109
p: 857.504.2900
f:617. 589.0914
ecog-acrin.org
November 10, 2022
Martha Kruhm, MS RAC
Head, Protocol and Information Office
Quality Assurance Section
CTEP, DCT, NCI
6130 Executive Blvd, EPN Room 7000
Bethesda, MD 20892
Dear Ms. Kruhm:
Enclosed is Addendum #31 to EAY131-V, MATCH Treatment Subprotocol V: Phase II Study of 
Sunitinib in Patients with Tumors with cKIT Mutations (Excluding GIST, Renal Cell Carcinoma or 
Pancreatic Neuroendocrine Tumor).
Please replace your current copy of the protocol and Informed Consent document with these 
updated versions. We recommend that each institution maintain a file containing the original 
protocol, Informed Consent, and all subsequent revisions/versions.
IRB Review Requirements:
This addendum has been reviewed and approved by the Central IRB, which is the sole 
IRB of record for this study. Local IRB review and approval is unnecessary.
Implementation of this addendum must occur on the activation date. Sites are not 
permitted to conduct the study utilizing outdated versions of any MATCH protocol documents 
after the activation date of this addendum.
The following revisions to the EAY131-V protocol have been made in this addendum:
Section
Change
1.
Cover Page
Updated Version Date and addendum number.
2.
Contact 
Page
Updated the phone number for the subprotocol chair, Dr. Lilian Gien.
The following revisions to the EAY131-V Informed Consent Document have been made in this 
addendum:
Section
Change
1.
Cover Page
Updated Version Date.
If you have any questions regarding this addendum, please contact eradomyshelsky@ecog-
acrin.org or 857-504-2900.

ii 
We request review and approval of this addendum to EAY131-V so ECOG-ACRIN may activate 
it promptly.   
Thank you.  
Sincerely, 
Pamela Cogliano 
Senior Director of Protocol Development 
 

EAY131-V
1
Molecular Analysis for Therapy Choice (MATCH)
MATCH Treatment Subprotocol V: Phase II Study of 
Sunitinib in Patients with Tumors with cKIT Mutations
(Excluding GIST, Renal Cell Carcinoma or Pancreatic 
Neuroendocrine Tumor)
SUNITINIB TREATMENT SUBPROTOCOL 
CHAIR:
Lilian T. Gien, MD
SUNITINIB TREATMENT SUBPROTOCOL CO-
CHAIR:
Andrew Poklepovic, MD
SUNITINIB TRANSLATIONAL CHAIR:
Eric Collisson, MD
Version Date: November 10, 2022
NCI Update Date:  August 12, 2015
NOTE: This subprotocol (EAY131-V) should be 
used in conjunction with the MATCH 
Master Protocol (EAY131).
SUBPROTOCOL ACTIVATION DATE
August 12, 2015 (Incorporated in Addendum #1)
Update #2 – 8/15
NOTE: As of 11/17, all protocol changes will be 
noted by addendum number.
Addendum #2 – 2/16
Addendum #3 – 5/16
Addendum #5 – 12/16
Addendum #7 – 3/17
Addendum #13
Addendum #19
Addendum #21
Addendum #25
Addendum #31
Agent
IND#
NSC#
Supply
Sunitinib malate
IND Sponsor: DCTD, NCI IND #: 126200
736511
NCI Supplied
Rev. Add13
Rev. Add19

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Table of Contents 
Molecular Analysis for Therapy Choice (MATCH) ...................................................... i 
MATCH Treatment Subprotocol V: Phase II Study of Sunitinib in Patients with 
Tumors with cKIT Mutations (Excluding GIST, Renal Cell Carcinoma or 
Pancreatic Neuroendocrine Tumor) ................................................................... 1 
Table of Contents ...................................................................................................... 2 
Schema ...................................................................................................................... 4 
1. Introduction ........................................................................................................ 5 
1.1 
Sunitinib Malate ........................................................................................ 5 
1.2 
Supporting Preliminary Data ................................................................... 11 
1.3 
Rationale ................................................................................................. 13 
1.4 
Objectives ................................................................................................ 13 
2. Selection of Patients ......................................................................................... 14 
2.1 
Eligibility Criteria ..................................................................................... 14 
3. Sunitinib Treatment Plan .................................................................................. 17 
3.1 
Administration Schedule ......................................................................... 17 
3.2 
Adverse Event Reporting Requirements ................................................. 17 
3.3 
Comprehensive Adverse Events and Potential Risks List (CAEPR) for 
Sunitinib malate (SU011248 L-malate, NSC 736511). ............................. 20 
3.4 
Dose Modifications ................................................................................. 26 
3.5 
General Concomitant Medications & Supportive Care Guidelines ......... 30 
3.6 
Duration of Agent-specific treatment ..................................................... 32 
3.7 
Duration of Follow-Up ............................................................................. 32 
4. Study Parameters .............................................................................................. 33 
4.1 
Therapeutic Parameters for Sunitinib Treatment ................................... 33 
5. Drug Formulation and Procurement ................................................................. 35 
5.1 
Sunitinib malate (NSC 736511) ............................................................... 36 
6. Translational Studies ......................................................................................... 38 
7. References ........................................................................................................ 38 
Appendix I  Patient Pill Calendar ............................................................................. 42 
Appendix II  Actionable Mutations of Interest (aMOIs) .......................................... 44 
Appendix III  Medications That May Cause QTc Prolongation ................................ 55 
Appendix IV  NCI/DCTD Collaborative Agreements Language ................................ 57 
Appendix V  Patient Clinical Trial Wallet Card ......................................................... 59 
 
 
 
Rev.12/16 
Rev. Add31 

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TREATMENT SUBPROTOCOL CHAIR 
Lilian T. Gien, MD 
Odette Cancer Centre, T2-104 
Sunnybrook Health Sciences Centre, 
2075 Bayview Avenue, 
Toronto, Ontario M4N 3M5, Canada 
Phone: 416-480-4026 
Fax: 416-480-6002 
Email: lilian.gien@sunnybrook.ca 
 
TREATMENT SUBPROTOCOL CO-CHAIR  
Andrew Poklepovic, MD 
Virginia Commonwealth University  
Massey Cancer Center 
McGlothlin Medical Education Center 
11th Floor room 215 
1201 East Marshall Street 
PO Box 980070 
Richmond Virginia 23298-0070 
Phone: 804-628-2321 
Email: apoklepovic@vcu.edu 
 
 
TRANSLATIONAL CHAIR 
Eric Collisson, MD 
University of California - San Francisco 
Department of Medicine 
1450 3rd St 
San Francisco, CA 94158-0128, 
Phone: 415-353-9888 
Email: eric.collisson@ucsf.edu 
 
 
 
 
 
 

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Schema 
 
 
Long-Term Follow-Up
Sunitinib 50 mg po daily x 28 days 
with 2 weeks (14 days) rest 
Until progression or unacceptable 
toxicity
Cycle = 42  days
Accrual Goal: 35
 
 

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1. 
Introduction 
1.1 
Sunitinib Malate 
Sunitinib malate (sunitinib; SU11248; SU011248; Sutent®) is an oral, multi-
targeted, small molecule inhibitor of the receptor tyrosine kinases (RTKs) 
involved in tumor proliferation and angiogenesis, including vascular endothelial 
growth factor receptor-1 (VEGFR-1), -2, and -3, platelet-derived growth factor 
receptor (PDGFR) -D and -E, stem cell factor receptor (KIT), the tyrosine kinase 
(TK) receptor encoded by the ret proto-oncogene (RET; rearranged during 
transfection), fms-like tyrosine kinase 3 (Flt3), basic fibroblast growth factor 
(bFGF) and colony-stimulating factor (CSF)-1R (O'Farrell et al., 2003a; Chow 
and Eckhardt, 2007; Faivre et al., 2007; Gan et al., 2009; Mashkani et al., 2010).  
Sunitinib selectively and potently inhibits the class III and class V split-domain 
RTKs (Mendel et al., 2003). 
Sunitinib was granted regulatory approval on January 26, 2006 by Food and 
Drug Administration (FDA) for the treatment of gastrointestinal stromal tumor 
(GIST) after disease progression on or intolerant to imatinib mesylate and 
accelerated approval for advanced renal cell carcinoma (RCC) (Goodman et al., 
2007; Izzedine et al., 2007; Rock et al., 2007), which was changed to regular 
approval on February 2, 2007. 
Mechanism of Action 
KIT-activating mutations 
Although in renal cell carcinoma the main mechanism of action of sunitinib is the 
inhibition of VEGF driven angiogenesis, sunitinib also exerts direct antitumor 
activity on cells that express target RTKs associated with tumor cell proliferation, 
such as KIT, PDGFR, and RET.    
KIT is a type III receptor tyrosine kinase that is important for the development of 
melanocytes, germ cells, mast cells, hematopoietic stem cells, and the interstitial 
cells of Cajal, the pacemaker cells of the gastrointestinal tract. Oncogenic KIT 
mutations result in ligand-independent kinase activation, leading to enhanced cell 
proliferation and survival [Hornick et al., 2007; Hoeben et al., 2008]. KIT-
activating mutations are found in 85-90% of GISTs [Heinrich et al., 2003], and it 
is now established that mutant KIT is a clinically important therapeutic target for 
this malignancy. 
KIT mutations have been found in several types of cancers.  For example, KIT 
mutations occur in almost all cases of systemic mastocytosis [Yavuz et al., 2002]. 
In subsets of acute myeloid leukemia, KIT mutations occur in 37% of adult cases 
[Park et al., 2011].  KIT mutations have also been observed in germ cell cancers, 
reported in up to 26% of testicular seminomas [Kemmer et al., 2004], and in 
approximately 30% of unilateral ovarian dysgerminomas [Hoei-Hansen et al., 
2007]. In melanoma, KIT mutations have been demonstrated in a small subset, 
mostly in those originating from mucosa, acral or chronic sun damaged sites 
[Beadling et al., 2008]. While KIT is also expressed in other tissues such as 
vascular endothelial cells, renal tubules, breast glandular epithelial cells, 
astrocytes, and sweat glands, recurrent mutations have not been described in 
these corresponding cancers, and early studies have failed to show efficacy of 

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KIT inhibitors in these entities, demonstrating the concept that a mutation or 
over-expression must be present in order for KIT to be a useful therapeutic target 
[Ashman et al., 2013]. 
There are multiple sites of KIT mutation in cancers. “Hot-spots” can correspond 
to the intracellular and extracellular juxtamembrane domains (exons 9, 11), the 
adenosine triphosphate (ATP) binding pocket of the receptor (exons 13, 14) and 
the activation loop of the kinase domain (exons 17, 18). Common sites of KIT 
mutation differ markedly between cancers. In GISTs, the most common region of 
KIT mutation is within exon 11 (65%), followed by exon 9 (15%), whereas 
mutations in exon 13 and 17 are uncommon (<5%) [Hornick et al., 2007]. In 
contrast, the most common KIT mutations in melanoma are within exons 11 and 
13 [Beadling et al.,. 2008], whereas hematopoietic malignancies and germ cells 
mainly have mutations in exon 17.  Figure X shows the mutation frequency 
across 80 cancer studies on the cBio portal http://bit.ly/1zCbcDi [PMID: 
22588877].  Of note, GIST is not included in this dataset. 
Sunitinib selectively inhibits KIT, as demonstrated by the clinical activity of this 
agent in patients with advanced or metastatic GIST. 
Nonclinical Specificity and Efficacy Studies 
In vitro studies have demonstrated the specificity of sunitinib for inhibition of the 
Class 3 and Class 5 RTKs, including receptors for VEGF (VEGFR), KIT, Flt-3, 
and PDGFR (Investigator’s Brochure, 2014).  Specifically, receptor 
phosphorylation inhibition studies have shown that sunitinib inhibits KIT-ligand-
induced phosphotyrosine levels in a dose-dependent manner with IC50 values of 
0.001-0.01 μM in vitro and reduced PDGFR-β phosphotyrosine levels in vivo 
(Abrams et al., 2003a).  Sunitinib also selectively inhibited proliferation of human 
umbilical vein endothelial cells (HUVEC) stimulated with VEGF (IC50=0.04 mcM) 
compared to FGF-stimulated proliferation (IC50=0.7 mcM) (Mendel et al., 2003). 
In animal efficacy studies, sunitinib showed broad antitumor activity in mouse 
xenograft models against a variety of human tumor cell lines including colorectal 
cancer (HT-29, Colo205), non-small cell lung cancer (H460), breast cancer 
(MDA-MB-435), melanoma (A375), epidermoid cancer (A431), and glioma 
(SF763T) (Mendel et al., 2003).  Sunitinib has also demonstrated antitumor 
activity against other breast cancer models (MMTV-v-Ha-ras transgenic mouse 
mammary carcinoma and dimethylbenzanthracene [DMBA]-induced rat 
mammary carcinomas) (Abrams et al., 2003b).  In an animal model of KIT-
expressing small cell lung cancer (SCLC; NCI-H526), sunitinib administration 
Figure 1:   

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resulted in greater tumor growth inhibition than did imatinib (Abrams et al., 
2003a). 
Additional nonclinical in vitro and in vivo studies are summarized in Chow and 
Eckhardt, 2007. 
Clinical Pharmacokinetics 
Orally-administered sunitinib is well absorbed in humans, with linear 
pharmacokinetics (PK) at doses of 50-150 mg/day (Sakamoto, 2004).  
Metabolism of sunitinib occurs primarily through the cytochrome P450 3A4 
(CYP3A4) to N-deethyl sunitinib to form the metabolite SU012662. SU012662 
undergoes further metabolism to an inactive metabolite SU014335. 
The PK of sunitinib and SU012662 were measured in a phase 1 dose-escalation 
study in patients with advanced solid malignancies (Faivre et al., 2006).  Twenty-
eight patients received doses ranging from 15 mg/m2 to 59 mg/m2 (ranging from 
50 mg every other day to 150 mg/day), on a 4 weeks on, 2 weeks off (4/2) 
schedule.  Overall, sunitinib displayed a long half-life and a large volume of 
distribution with moderate interpatient variability. At the recommended dose, Cmax 
occurred approximately 5 hours after administration and t1/2 ranged from 41-86 
hours. Doses of 50 mg daily led to plasma concentrations ranging from 50-100 
ng/mL.  
Fixed dosing on a milligram basis was considered appropriate for phase 2 
studies (Faivre et al., 2006). 
To determine the effect of food on the PK of sunitinib and its active metabolite 
SU012662, 16 healthy subjects received a single dose of sunitinib 50 mg under 
fasting conditions and 14 subjects received a single dose of sunitinib 50 mg 
under fed conditions. Sunitinib and SU012662 half-lives, and oral clearance of 
sunitinib, were not affected by food (Bello et al., 2006). 
A study of sunitinib PK in patients with AML indicated that a plasma 
concentration of 50-100 ng/mL of combined sunitinib and SU012662 could be 
achieved on the first cycle of a 50 mg/day 4/2 regimen, similar to that achieved in 
studies with patients having other tumor types (Fiedler et al., 2005). 
Population PK methods indicated that the covariates of weight, gender, race, 
ethnicity, ECOG score, and tumor type had no clinically significant effects on 
drug exposure, and that adjustments of starting doses based on these covariates 
were not required (Investigator’s Brochure, 2014). 
Concurrent administration of a single dose of sunitinib with ketoconazole (a 
strong CYP3A4 inhibitor) in healthy volunteers resulted in 49% and 51% 
increases in the combined (sunitinib + SU012662) Cmax and AUC0-∞ values, 
respectively, compared with sunitinib alone (Washington et al., 2003).  
Concurrent administration of sunitinib and rifampin (a strong CYP3A4 inducer) in 
healthy subjects resulted in 23% and 46% reduction in combined Cmax and  
AUC0-∞, respectively, compared with sunitinib alone (Bello et al., 2005). Thus, 
dose adjustments for sunitinib should be considered when coadministered with 
strong CYP3A4 inhibitors and inducers. 

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Proposed Dose and Schedule for Phase 2 Clinical Trials 
Starting doses in multiple-dose studies were 25, 50, 75, and 100 mg 
administered orally once daily with the majority of patients receiving the 50-mg 
dose.  Patients in sunitinib studies have been treated on four different schedules: 
schedules 4/1 and 4/2 comprised 4 consecutive weeks of daily dosing followed 
by a 1- or 2-week rest period, respectively, while schedules 2/1 and 2/2 
comprised 2 consecutive weeks of daily dosing followed by a 1- or 2-week rest 
period, respectively.  The majority of subjects were treated on schedules 4/2 or 
2/2 in phase 1 studies.  Schedule 4/2 has been well tolerated with generally mild 
to moderate adverse effects at a 50 mg daily dose.   Alternate regimens of 
sunitinib are being explored; 50 mg of sunitinib daily for 2 weeks followed by a 1-
week off-treatment period (sunitinib 2/1) (Britten et al., 2008), while another 
schedule is sunitinib 37.5 mg as a CDD (George et al., 2008).  Both schedules 
were well-tolerated, achieved therapeutic plasma concentrations and showed no 
significant accumulation of the drug. This study will use the most common dosing 
schedule of sunitinib, 50mg po daily for 4 weeks, followed by 2 weeks rest. 
Safety Profile 
Sunitinib is reasonably well tolerated, with asthenia, hypertension, dermatitis, and 
mild myelosuppression as the most common AEs (Stadler, 2006). The most 
common adverse reactions (≥ 20%) are fatigue, asthenia, fever, diarrhea, 
nausea, mucositis/stomatitis, vomiting, dyspepsia, abdominal pain, constipation, 
hypertension, peripheral edema, rash, plantar palmar erythrodysesthesia (PPE, 
hand-foot syndrome), skin discoloration, dry skin, hair color changes, altered 
taste, headache, back pain, arthralgia, extremity pain, cough, dyspnea, anorexia, 
and bleeding (Sutent Prescribing Information, 2014). Additionally, the inhibition of 
TK receptors by agents such as sunitinib can result in cutaneous AEs such as 
acral erythema, subungal splinter hemorrhages, modification of hair and skin 
pigmentation, mucositis, and (occasionally) periocular edema (Robert et al., 
2005; Suwattee, 2008). PPE is characterized by inflammation, hyperkeratosis, 
blistering, and pain in the hands and/or feet of patients, usually bilaterally, which 
can occur in patients receiving sunitinib (Porta et al., 2007; Suwattee, 2008).  A 
recent analysis of dermatological AEs in patients receiving sunitinib therapy has 
reported that all-grade PPE reactions occurred in 19% of patients (5% grades 3-
4), skin discoloration in 28% (no grades 3-4), dry skin in 16% (1% grades 3-4), 
skin rash in 13% (1% grades 3-4), dermatitis in 8% (2% grades 3-4), hair color 
changes in 10% (no grades 3-4), alopecia in 6% (no grades 3-4), and 
phototoxicity in < 0.1% (no grades 3-4) (Rosenbaum et al., 2008). 
Hepatotoxicity, which can lead to liver failure and possible death, has been 
associated with sunitinib. Liver failure has been observed in clinical trials (7/2281 
[0.3%]) and post-marketing experience, leading to a boxed label warning. Liver 
failure signs include jaundice, elevated transaminases and/or hyperbilirubinemia 
in conjunction with encephalopathy, coagulopathy, and/or renal failure. The 
incidence of low-grade and high-grade elevations of AST and ALT is reported to 
be 40-60%, and grade 3-4 elevations to be 2-5% [Shah et al., 2013]. It is 
recommended that liver function tests be monitored prior to initiating treatment, 
during each cycle, and as clinically indicated. Sunitinib should be interrupted for 
grade 3 or 4 drug-related hepatic adverse events and discontinued if there is no 
resolution. 

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Cardiotoxicity, including congestive heart failure (3%-8%) and left ventricular 
dysfunction (12%-14%), has been reported in patients undergoing treatment with 
sunitinib (Chu et al., 2007; Khakoo et al., 2008; Schmidinger et al., 2008; Telli et 
al., 2008).  More subjects treated with sunitinib experienced decline in left 
ventricular ejection fraction (LVEF) than subjects receiving either placebo or IFN-
α (Investigator’s Brochure, 2014). In clinical trials, decreases in LVEF of ≥20% 
and below the lower limit of normal (LLN) occurred in approximately 2% of 
sunitinib-treated GIST patients, 4% of cytokine-refractory MRCC patients and 2% 
of placebo-treated patients. These LVEF declines do not appear to have been 
progressive and often improved as treatment continued. In the treatment-naive 
MRCC study, 27% and 15% of subjects on sunitinib and IFN-α, respectively, had 
an LVEF value below the LLN. Two patients (< 1%) who received sunitinib were 
diagnosed with congestive heart failure (CHF). Among 461 patients enrolled in 
CDUS-monitored trials with sunitinib alone, 2% of patients experienced left 
ventricular systolic dysfunction (CDUS data).  It is unknown whether patients with 
concurrent cardiac conditions may be at a higher risk for developing drug-related 
LVEF.  Baseline and periodic evaluations of LVEF should be considered when 
clinically indicated while these patients are on sunitinib treatment.  In patients 
without cardiac risk factors, a baseline evaluation of LVEF should be considered 
when clinically indicated. 
Sunitinib has been shown to prolong the QT interval in a dose-dependent 
manner, which may lead to an increased risk for ventricular arrhythmias, 
including Torsade de Pointes.  This condition has been reported in <0.1% of 
sunitinib-exposed patients.  The DCTD, NCI, issued an IND AE Action Letter to 
all investigators using sunitinib describing the occurrence of QTc prolongation 
and Torsade de pointes (ventricular tachycardia) in patients on clinical trials 
utilizing sunitinib.  As a result of this Action Letter, DCTD, NCI-sponsored 
sunitinib protocols were amended to include the requirement for a baseline EKG 
prior to study treatment, exclude patients with histories of serious ventricular 
arrhythmias or prolonged QTc, and exclude patients with certain cardiac 
conditions. 
Treatment-related hypertension was reported in clinical trials in subjects with 
solid tumors, including primarily GIST and cytokine-refractory RCC. Sunitinib 
dosing was reduced or temporarily delayed in approximately 2.7% of this patient 
population. None of these patients were discontinued from treatment with 
sunitinib. Severe hypertension (> 200 mmHg systolic or 110 mmHg diastolic) 
occurred in 4.7% of this patient population. Of subjects receiving sunitinib for 
treatment-naive MRCC, 33.9% receiving sunitinib experienced hypertension, 
compared with 3.6% on IFN-α.  Severe hypertension occurred in 12% of 
treatment-naive patients on sunitinib compared to <1% on IFN-α.  Hypertension 
was reported in 26.5% of patients receiving sunitinib in a Phase 3 pNET study, 
compared to 4.9% of patients receiving placebo. Severe hypertension occurred 
in 10% of pNET patients on sunitinib and 3% of patients on placebo 
(Investigator’s Brochure, 2014).  Among 516 patients enrolled in CDUS-
monitored trials with sunitinib alone, 33.9% experienced hypertension (CDUS 
data). Patients should be screened for hypertension and controlled as 
appropriate. Temporary suspension is recommended in patients with severe 
hypertension that is not controlled with medical management. Treatment may be 
resumed once hypertension is appropriately controlled. 
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In subjects receiving sunitinib for treatment-naive MRCC, 39% had bleeding 
events compared with 11% receiving IFN-α (Investigator’s Brochure, 2014).  
Treatment emergent bleeding events occurred in 18% of patients receiving 
sunitinib in the double-blind treatment phase of the GIST phase 3 study, 
compared with 17% receiving placebo. Seventeen (4.5%) patients on sunitinib 
versus 5 (1.7%) patients on IFN-α experienced Grade 3 or greater treatment-
related bleeding events. Of patients receiving sunitinib for cytokine-refractory 
MRCC (C-R MRCC), 26% experienced bleeding. Bleeding events, excluding 
epistaxis, occurred in 21.7% of patients receiving sunitinib in the Phase 3 pNET 
study compared to 9.85% of patients receiving placebo. Routine assessment of 
this event should include complete blood counts and physical examination. 
Among 516 patients enrolled in CDUS-monitored trials with sunitinib alone or in 
combination with other agents, there were 123 reported bleeding events (CDUS 
data).  Epistaxis was the most common hemorrhagic AE reported.  Tumor-related 
hemorrhage can occur with sunitinib and in the case of pulmonary tumors, may 
present as severe and life-threatening hemoptysis or pulmonary hemorrhage. 
Thyroid dysfunction has been reported with sunitinib. Hypothyroidism has been 
reported in 71% patients with RCC (Rini et al., 2007) and in 36% of those with 
GIST (Desai et al, 2006) treated with sunitinib.  Acquired hypothyroidism was 
noted in 6.2% of GIST patients on sunitinib versus 1% on placebo. 
Hypothyroidism was reported as an adverse event in 16% of patients on sunitinib 
in the treatment-naive MRCC study and three patients (< 1%) in the IFN-α arm, 
and in 4% of patients across the two cytokine-refractory MRCC studies. 
Additionally, TSH elevations were reported in 2% of cytokine-refractory MRCC 
patients. Overall, 7% of the cytokine-refractory MRCC population had either 
clinical or laboratory evidence of treatment-emergent hypothyroidism. In the 
Phase 3 pNET study, treatment-related hypothyroidism was reported in 6 
patients (7.2%) receiving sunitinib and in one patient (1.2%) on placebo. Cases 
of hyperthyroidism have been reported in clinical trials and through post-
marketing experience (Investigator’s Brochure, 2014).  Baseline measurement of 
thyroid function is recommended, and patients with thyroid dysfunction should be 
treated appropriately prior to starting sunitinib therapy. All patients should be 
observed closely for signs and symptoms of thyroid dysfunction on sunitinib 
treatment. Patients with signs and/or symptoms suggestive of hypothyroidism or 
hyperthyroidism should have laboratory monitoring of thyroid function performed 
and be treated as per standard medical practice. 
Hypoglycemia has also been reported with sunitinib therapy. General guidelines 
recommend checking blood glucose levels regularly and assessment if anti-
diabetic drug dose modifications are required (Sutent Prescribing Information, 
2014). 
Nonclinical evidence of adrenal toxicity following sunitinib exposure led the 
company to perform specialized safety assessments in clinical studies, including 
computed tomography or MRI in 336 subjects to specifically identify any change 
in adrenal gland structure or the presence of adrenal gland hemorrhage 
(Investigator’s Brochure, 2014).  Neither event was observed.  
Adrenocorticotropic hormone (ACTH) stimulation testing was done in 400 
patients across multiple sunitinib trials.  One subject developed consistently 
abnormal test results during treatment that were unexplained and may be related 
to sunitinib treatment.  Eleven additional subjects had abnormalities in the final 

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test, with low peak cortisol levels.  None of these patients had clinical evidence of 
adrenal insufficiency.  However, based on the nonclinical findings, patients 
receiving sunitinib should be clinically followed for signs and symptoms of 
adrenal insufficiency, especially in (1) patients with comorbidities associated with 
adrenal dysfunction, (2) patients with preexisting adrenal insufficiency (primary or 
secondary), and (3) patients with concomitant stress (e.g., fever, infection, 
bleeding, serious accident, surgery) that may precipitate overt adrenal 
insufficiency in the presence of subclinical sunitinib-induced adrenal toxicity. 
Serum chemistries including phosphate should be performed at the beginning of 
each treatment cycle.  Supportive care may include anti-emetic premedication, 
supportive oral care products, and analgesics.  Serious complications due to 
degeneration or shrinkage of tumors, including tumor lysis syndrome, 
gastrointestinal perforation and tracheoesophageal fistula, have occurred rarely 
in patients with abdominal, head and neck, thyroid, and other malignancies 
treated with sunitinib, believed to be the result of the antitumor effect of sunitinib.  
Other serious effects include thromboembolic events, rare reversible posterior 
leukoencephalopathy syndrome (RPLS), proteinuria with rare nephrotic 
syndrome, and rare microangiopathic hemolytic anemia.  
Management of treatment related adverse events is discussed in greater detail in 
Section 3.4. 
1.2 
Supporting Preliminary Data  
Clinical Experience 
As of 01 October 2012, 13026 subjects with solid malignant tumors had received 
at least one dose of sunitinib in multiple-dose studies, and for 12801 of these 
13026 (98.3%) subjects, safety data is available (Investigator’s Brochure, 2014).  
In phase 1 studies, sunitinib demonstrated single-agent activity in patients with 
RCC, GIST, non-GIST sarcomas, non-small cell lung cancer (NSCLC), colorectal 
cancer, neuroendocrine tumors (NET), melanoma, prostate cancer, and thyroid 
cancer.  Sunitinib has also been studied in the phase 1 setting in patients with 
acute myeloid leukemia (AML).  Pivotal trials of sunitinib in imatinib-resistant 
GIST (a placebo-controlled phase 3 trial), and metastatic RCC (MRCC) (single-
arm, non-randomized, multicenter, open-label trial) and supporting trials in each 
disease were completed and submitted in support of the New Drug Application 
(NDA).  In addition, there are several ongoing company-sponsored single agent 
and combination clinical trials for a variety of other indications. 
Sunitinib as a therapy for tumors with KIT-mutations 
The majority of data supporting the use of sunitinib for KIT mutations has been 
studied in GISTs. The tyrosine-kinase inhibitor (TKI) imatinib is established as 
the standard therapy for metastatic GIST, and has been associated with 
substantial improvements in overall survival. However, after an initial benefit from 
imatinib, the vast majority of patients eventually develop disease progression or 
secondary resistance. Sunitinib, which also selectively inhibits KIT, has 
demonstrated clinical benefit for patients who progress on imatinib therapy.  In a 
phase III trial of sunitinib vs. placebo, 312 GIST patients with confirmed 
progression on previous imatinib therapy were randomized in a 2:1 ratio to 
receive sunitinib (n=207) or placebo (n=105); the trial was unblinded early when 
a planned interim analysis showed significantly longer time to tumor progression 

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with sunitinib. Median time to tumor progression was 27.3 weeks (95% CI 16.0–
32.1) in patients receiving sunitinib and 6.4 weeks (4.4–10.0) in those on placebo 
(hazard ratio 0.33; p<0.0001). Therapy was reasonably well tolerated; the most 
common adverse events were fatigue, diarrhea, skin discoloration and nausea 
[Demetri et al., 2006]. This trial led to FDA-approval of sunitinib as a treatment 
option for patients with imatinib resistant tumors. 
Recent studies have shown that sunitinib may have activity in patients with other 
tumors that have c-KIT mutations, such as melanoma. There are three phase II 
studies demonstrating response to imatinib for melanomas harboring KIT 
mutations of approximately 20-29% [Carvajal et al., 2011, Guo et al., 2011, Hodi 
et al., 2013].  In a phase II study of sunitinib in melanoma patients, of the four 
evaluable patients with KIT mutations, 1 had a complete remission for 15 months 
and 2 had partial responses (1- and 7-month duration) [Minor et al., 2012]. The 
tolerability and toxicity of sunitinib was similar to that reported in renal cell cancer 
and GISTs. 
Efficacy according to genotype 
It is known that GIST responsiveness to imatinib varies by primary KIT genotype; 
exon 11-mutant GISTs are more sensitive to imatinib than exon 9-mutant GISTs. 
Heinrich et al. (2008) conducted a study which evaluated the clinical activity of 
sunitinib based on GIST kinase genotype. When evaluating primary tumor 
genotype, the objective response to sunitinib was more common in patients with 
KIT exon 9 than exon 11 mutant GISTs (37% vs 5%, p=0.002), and the median 
progression-free survival (PFS) was significantly longer for patients with exon 9 
mutations compared to those with exon 11 mutations (19.4 months vs 5.1 
months, p=0.0005). Median overall survival was also significantly longer for 
patients with exon 9 mutations (26.9 months vs 12.3 months, p=0.012). Among 
those with secondary tumor genotype, clusters of mutations occurred in exons 13 
and 14, as well as exon 17. The median PFS with sunitinib was significantly 
longer for those with secondary KIT exon 13 or 14 mutations, than for those with 
exon 17 or 18 mutations (7.8 months vs 2.3 months, p=0.016). Furthermore, 
Gajiwala et al. (2009) demonstrated biochemically that GISTs with exon 17 
mutations are strongly resistant to sunitinib. These mutants bind sunitinib in the 
inactivated form but are then converted to the active drug-resistant form. We will 
exclude patients with exon 17 and 18 cKIT mutations from this trial. 
KIT inhibitors in other malignancies 
Other than in GIST and melanoma, sunitinib has not been studied systematically 
as a therapy against the KIT mutation in other malignancies. Early trials of 
imatinib in unselected cases of acute myeloid leukemia (AML) have been 
unsuccessful, likely due to the low rate of KIT mutations of 7%, and the 
frequency of resistant mutations on the activation loop of the kinase domain 
[Piccaluga et al., 2007]. However, small studies have suggested that 
identification of particular mutations in AML may select a subgroup of patients 
who are more likely to respond [Cairoli et al., 2005]. Imatinib has also been used 
in cases of systemic mastocytosis, but the heterogeneous group of patients leads 
to difficulty in adequately evaluating response to therapy. Additionally, activation 
loop mutations are found in the majority of patients with systemic mastocytosis. 
Use of imatinib may be more effective in those cases negative for the activation 
loop mutations [Orfao et al., 2007]. Imatinib has also been tested in breast 

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cancer cell lines and testicular seminoma cell lines with encouraging results 
[Roussidis et al., 2007; Kemmer et al., 2004]. 
1.3 
Rationale 
Although sunitinib has anti-angiogenic properties and has activity against several 
kinases, Sunitinib has been approved for patients with metastatic GIST who are 
resistant to imatinib. Few studies have evaluated sunitinib in melanomas with 
cKIT mutations, but response has been observed, and otherwise this agent has 
not been evaluated in other malignancies with cKIT mutations. The numbers of 
patients with a cKIT mutation in each type of malignancy is relatively small, 
making it difficult to establish response among specific types of malignancies. 
The MATCH trial aims to establish whether patients whose tumors harbor 
mutations in specific pathways of interest benefit (as defined as objective 
response) from agents targeting that pathway, irrespective of tumor type. This 
trial will allow detection of a sufficient cohort of patients to determine the effect of 
sunitinib on tumors with cKIT mutations, and allow investigation of whether 
agents likely to have activity against a molecular alteration in one disease will 
exhibit similar activity in other diseases with the same molecular alterations. 
1.4 
Objectives 
Primary:  
a) Observe response rate in patients with c-KIT mutations treated with sunitinib 
Secondary: 
a) Observe 6-month progression free survival of patients with c-KIT mutations 
treated with sunitinib  
b) Observe time to progression of patients with c-KIT mutations treated with 
sunitinib 
c) Document toxicities in patients with c-KIT mutations treated with sunitinib 
 

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2. 
Selection of Patients 
Each of the criteria in the checklist that follows must be met, along with the eligibility in 
the MATCH Master Protocol, in order for a patient to be considered eligible for this 
study. Use the checklist to confirm a patient’s eligibility. For each patient, this checklist 
must be photocopied, completed and maintained in the patient’s chart.  
In calculating days of tests and measurements, the day a test or measurement is 
done is considered Day 0. Therefore, if a test is done on a Monday, the Monday 
four weeks later would be considered Day 28.  
ECOG-ACRIN Patient No. ____________________________ 
Patient’s Initials (L, F, M) _______________________ 
Physician Signature and Date ___________________ 
NOTE: 
Policy does not allow for the issuance of waivers to any protocol specified 
criteria (http://ctep.cancer.gov/protocolDevelopment/policies_deviations.htm). 
Therefore, all eligibility criteria listed in Section 2 must be met, without 
exception. The registration of individuals who do not meet all criteria listed in 
Section 2 can result in the participant being censored from the analysis of the 
study, and the citation of a major protocol violation during an audit.  All 
questions regarding clarification of eligibility criteria must be directed to the 
Group's Executive Officer (EA.Execofficer@jimmy.harvard.edu) or the 
Group's Regulatory Officer (EA.RegOfficer@jimmy.harvard.edu). 
NOTE: 
Institutions may use the eligibility checklist as source documentation if it has 
been reviewed, signed, and dated prior to registration/randomization by the 
treating physician. 
NOTE: 
All patients must have signed the relevant treatment consent form 
2.1 
Eligibility Criteria  
2.1.1 
Patients must fulfill all eligibility criteria outlined in Section 3.1 of 
MATCH Master Protocol (excluding Section 3.1.6) at the time of 
registration to treatment step (Step 1, 3, 5, 7). 
2.1.2 
Patients must have a somatic cKIT mutation in exon 9, 11, 13 or 14, 
excluding exon 17 or 18 mutations, activating PDGFRA or PDGFRB 
variants and fusions, or another aberration, as identified via the MATCH 
Master Protocol and described in Appendix II. See Appendix II 
 
Actionable Mutations of Interest (aMOIs)for information on the 
inclusion and exclusion mutations, along with the corresponding 
Levels of Evidence (LOE). 
2.1.3 
Patient must have normal organ and marrow function as defined 
below: 
x 
Total bilirubin must be within normal institutional limits. 
x 
Creatinine must be within normal institutional limits. 
OR 
_____ 
_____ 
_____ 
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Creatinine clearance ≥ 60 mL/min/1.73 m2 for patients with 
creatinine levels above institutional normal. 
Creatinine Clearance:   
 
x 
Serum Calcium must be ≤ 12.0 mg/dL. 
2.1.4 
Patients must have an electrocardiogram (ECG) within 8 weeks prior 
to treatment assignment and must have no clinically important 
abnormalities in rhythm, conduction or morphology of resting ECG 
(e.g. complete left bundle branch block, third degree heart block): 
Date of ECG:  _______________ 
2.1.5 
Patients with known left ventricular dysfunction must have ECHO or a 
nuclear study (MUGA or First Pass) within 4 weeks prior to 
registration to treatment and must not have left ventricular ejection 
fraction (LVEF) < institutional lower limit of normal (LLN). If the LLN is 
not defined at a site, the LVEF must be > 50% for the patient to be 
eligible. 
2.1.5.1 
The following groups of patients are eligible provided they 
have New York Heart Association Class II cardiac function 
on baseline ECHO/nuclear study: 
x 
Patients with a history of Class II heart failure who are 
asymptomatic on treatment 
x 
Patients with prior anthracycline exposure 
x 
Patients who have received central thoracic radiation 
that included the heart in the radiotherapy port 
Date of ECHO/nuclear study:  _______________ 
NOTE: 
Pre-treatment LVEF determination in patients without 
known left ventricular dysfunction (or per Section 2.1.5.1) 
is NOT otherwise required. 
2.1.6 
Patients with any of the following conditions are excluded: 
x 
Serious or non-healing wound, ulcer, or bone fracture 
x 
History of abdominal fistula, gastrointestinal perforation, or intra-
abdominal abscess within 28 days of treatment 
x 
Any history of cerebrovascular accident (CVA) or transient 
ischemic attack within 12 months prior to study entry 
x 
History of myocardial infarction, cardiac arrhythmia, 
stable/unstable angina, symptomatic congestive heart failure, or 
coronary/peripheral artery bypass graft or stenting within 12 
months prior to study entry 
x 
History of pulmonary embolism within the past 12 months 
2.1.7 
Patients must not have known hypersensitivity or excess toxicity from 
sunitinib or compounds of similar chemical composition or biologic 
effect.  This list includes, but is not limited to, patients with significant 
cardiac or hepatic toxicity from multikinase inhibitors with similar 
kinase inhibitory profiles (sorafenib, regorafenib, pazopanib). 
_____ 
_____ 
_____ 
_____ 
_____ 
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Questions regarding a significant intolerance to a prior therapy should 
be directed to the sub-protocol PI.     
2.1.8 
Patients must not have had prior therapy with sunitinib. 
2.1.9 
Patients must not have planned ongoing administration of STRONG 
and MODERATE CYP3A4 inhibitors or inducers. See Appendix V 
(and Appendix VI of the MATCH Master Protocol). The reference list 
of cytochrome p450 (CYP) isozymes and classification of strong, 
moderate, and weak interactions is available through the FDA 
website: 
http://www.fda.gov/Drugs/DevelopmentApprovalProcess/Development
Resources/DrugInteractionsLabeling/ucm093664.htm 
x 
Strong CYP3A4 inhibitors are not permitted within 7 days before 
dosing and should be avoided throughout the study. 
x 
Strong CYP3A4 inducers are not permitted within 12 days before 
dosing and should be avoided throughout the study. 
2.1.10 
Patients must not have GIST, renal cell carcinoma, or pancreatic 
neuroendocrine tumor 
2.1.11 
Patients must not have a NCI CTCAE version 4 grade 3 hemorrhage 
within 4 weeks of starting study treatment 
2.1.12 
Patients must not have hypertension that cannot be controlled by 
medications (> 140/90 mmHg despite optimal medical therapy) 
2.1.13 
Patients must not have pre-existing thyroid abnormality with thyroid 
function that cannot be maintained in the normal range with 
medication 
2.1.14 
Participants may not have a major surgical procedure, open biopsy, or 
significant traumatic injury within 28 days prior to starting sunitinib. 
2.1.15 
Patients with known brain metastases should be excluded from this 
clinical trial because of their poor prognosis and because they often 
develop progressive neurologic dysfunction that would confound the 
evaluation of neurologic and other adverse events. 
2.1.16 
Patients who require therapeutic doses of coumarin derivative 
anticoagulants such as warfarin are excluded, although doses up to 2 
mg daily are permitted for prophylaxis of thrombosis. 
NOTE: 
Low molecular weight heparin is permitted provided that 
the patient’s PT INR is < 1.5. 
 
 
 
 
 
Physician Signature 
 
Date 
OPTIONAL: 
This signature line is provided for use by institutions wishing to 
use the eligibility checklist as source documentation. 
 
_____ 
_____ 
_____ 
_____ 
_____ 
_____ 
_____ 
_____ 
_____ 

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NCI Update Date: August 12, 2015 
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3. 
Sunitinib Treatment Plan 
3.1 
Administration Schedule 
Sunitinib is dosed at 50mg po, daily, regardless of ideal or actual body weight. 
3.1.1 
Sunitinib 
50mg po, daily, for 4 weeks continuously, followed by 2 weeks of rest. 
Repeat at 6 week cycles until progression or patient is withdrawn from 
study, as outlined in Section 3.6. 
3.1.2 
Dose interruptions and modifications will be performed according to 
guidelines outlined in Section 3.4 
3.2 
Adverse Event Reporting Requirements 
The Adverse Event Reporting Requirements for all EAY131 subprotocols are 
outlined in the MATCH MASTER protocol.  Please refer to those guidelines when 
determining if an event qualifies as a Serious Adverse Event (SAE) and requires 
expedited reporting via CTEP’s Adverse Event Reporting System (CTEP-AERS). 
In addition, the following section outlines agent specific requirements and must 
be followed to ensure all reporting requirements are met. 
3.2.1 
Additional instructions, requirements and exceptions for protocol 
EAY131 – Subprotocol V 
Additional Instructions 
For instructions on how to specifically report events that result in 
persistent or significant disability/incapacity, congenital anomaly, 
or birth defect events via CTEP-AERS, please contact the AEMD 
Help Desk at aemd@tech-res.com  or 301-897-7497. This will 
need to be discussed on a case-by-case basis. 
 
EAY131 – Subprotocol V specific expedited reporting 
requirements: 
x 
Pregnancies: Pregnancies and suspected pregnancies 
(including a positive or inconclusive pregnancy test, regardless 
of age or disease state) occurring while the female patient is on 
Sunitinib, or within 28 days of the female patient’s last dose of 
Sunitinib, are considered immediately reportable events. The 
pregnancy, suspected pregnancy, or positive/ inconclusive 
pregnancy test must be reported via CTEP-AERS within 24 
hours of the Investigator’s knowledge.  Please refer to 
Appendix VIII in MATCH Master Protocol for detailed 
instructions on how to report the occurrence of a pregnancy as 
well as the outcome of all pregnancies. 
 
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NCI Update Date: August 12, 2015 
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EAY131 – Subprotocol V specific expedited reporting 
exceptions: 
For Subprotocol V, the adverse events listed below do not require 
expedited reporting via CTEP-AERS: 
x 
If an AE meets the reporting requirements of the protocol, and 
it is listed on the SPEER, it should ONLY be reported via 
CTEP-AERS if the grade being reported exceeds the grade 
listed in the parentheses next to the event 
3.2.2 
Second Primary Cancer Reporting Requirements 
All cases of second primary cancers, including acute myeloid 
leukemia (AML) and myelodysplastic syndrome (MDS), that occur 
following treatment on NCI-sponsored trials must be reported to 
ECOG-ACRIN using Medidata Rave 
x 
A second malignancy is a cancer that is UNRELATED to any 
prior anti-cancer treatment (including the treatment on this 
protocol).  Second malignancies require ONLY routine reporting 
as follows: 
1. Complete a Second Primary Form in Medidata Rave within 14 
days. 
2. Upload a copy of the pathology report to ECOG-ACRIN via 
Medidata Rave confirming the diagnosis. 
3. If the patient has been diagnosed with AML/MDS, upload a 
copy of the cytogenetics report (if available) to ECOG-ACRIN 
via Medidata Rave. 
x 
A secondary malignancy is a cancer CAUSED BY any prior anti-
cancer treatment (including the treatment on this protocol). 
Secondary malignancies require both routine and expedited 
reporting as follows: 
1. Complete a Second Primary Form in Medidata Rave within 14 
days 
2. Report the diagnosis via CTEP-AERS at http://ctep.cancer.gov  
Report under a.) leukemia secondary to oncology 
chemotherapy, b.) myelodysplastic syndrome, or c.) 
treatment related secondary malignancy 
3. Upload a copy of the pathology report to ECOG-ACRIN via 
Medidata Rave and submit a copy to NCI/CTEP confirming the 
diagnosis. 
4. If the patient has been diagnosed with AML/MDS, upload a 
copy of the cytogenetics report (if available) to ECOG-ACRIN 
via Medidata Rave and submit a copy to NCI/CTEP. 
NOTE: 
The Second Primary Form and the CTEP-AERS report 
should not be used to report recurrence or development of 
metastatic disease. 

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NOTE: 
If a patient has been enrolled in more than one NCI-
sponsored study, the Second Primary Form must be 
submitted for the most recent trial. ECOG-ACRIN must be 
provided with a copy of the form and the associated 
pathology report and cytogenetics report (if available) even 
if ECOG-ACRIN was not the patient's most recent trial. 
NOTE: 
Once data regarding survival and remission status are no 
longer required by the protocol, no follow-up data should 
be submitted via CTEP-AERS or by the Second Primary 
Form. 

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3.3 
Comprehensive Adverse Events and Potential Risks List (CAEPR) for Sunitinib 
malate (SU011248 L-malate, NSC 736511). 
The Comprehensive Adverse Events and Potential Risks list (CAEPR) provides a 
single list of reported and/or potential adverse events (AE) associated with an 
agent using a uniform presentation of events by body system. In addition to the 
comprehensive list, a subset, the Specific Protocol Exceptions to Expedited 
Reporting (SPEER), appears in a separate column and is identified with bold and 
italicized text. This subset of AEs (SPEER) is a list of events that are protocol 
specific exceptions to expedited reporting to NCI (except as noted below).  Refer 
to the 'CTEP, NCI Guidelines: Adverse Event Reporting Requirements' 
http://ctep.cancer.gov/protocolDevelopment/electronic_applications/docs/aeguide
lines.pdf for further clarification. Frequency is provided based on 7115 patients. 
Below is the CAEPR for Sunitinib malate (SU011248 L-malate). 
NOTE: 
If an AE meets the reporting requirements of the protocol, and it is 
listed on the SPEER, it should ONLY be reported via CTEP-AERS if 
the grade being reported exceeds the grade listed in the parentheses 
next to the event in the SPEER. 
Version 2.14, February 15, 20191 
 
Adverse Events with Possible 
Relationship to Sunitinib malate (SU011248 L-malate) 
(CTCAE 5.0 Term) 
[n= 7115] 
 
 
Specific Protocol 
Exceptions to Expedited 
Reporting (SPEER) 
Likely (>20%) 
Less Likely (<=20%) 
Rare but Serious (<3%)   
BLOOD AND LYMPHATIC SYSTEM DISORDERS 
  
 
Anemia 
 
 Anemia (Gr 3) 
 
 
Hemolytic uremic 
syndrome 
  
 
 
Thrombotic 
thrombocytopenic purpura   
CARDIAC DISORDERS 
  
 
 
Cardiac disorders - Other 
(cardiomyopathy) 
  
 
 
Heart failure 
  
 
 
Left ventricular systolic 
dysfunction 
  
 
 
Myocardial infarction 
  
ENDOCRINE DISORDERS 
  
 
 
Endocrine disorders - 
Other (thyroiditis) 
  
 
 
Hyperthyroidism 
  
 
Hypothyroidism 
 
 Hypothyroidism (Gr 2) 
EYE DISORDERS 
  
 
 
Eye disorders - Other 
(macular edema) 
 Eye disorders - Other 
(macular edema) (Gr 2) 
 
 Papilledema 
 
 Papilledema (Gr 2) 
 
 
Vision decreased 
 Vision decreased (Gr 2) 
Rev. 5/16 
Rev. 3/17 
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Adverse Events with Possible 
Relationship to Sunitinib malate (SU011248 L-malate) 
(CTCAE 5.0 Term) 
[n= 7115] 
 
 
Specific Protocol 
Exceptions to Expedited 
Reporting (SPEER) 
Likely (>20%) 
Less Likely (<=20%) 
Rare but Serious (<3%)   
GASTROINTESTINAL DISORDERS 
  
 
Abdominal distension 
 
 Abdominal distension (Gr 
2) 
Abdominal pain 
 
 
 Abdominal pain (Gr 3) 
Anal mucositis 
 
 
 Anal mucositis (Gr 2) 
Constipation 
 
 
 Constipation (Gr 2) 
Diarrhea 
 
 
 Diarrhea (Gr 3) 
 
Dry mouth 
 
 Dry mouth (Gr 2) 
Dyspepsia 
 
 
 Dyspepsia (Gr 2) 
 
 
Esophagitis 
  
 
Flatulence 
 
 Flatulence (Gr 2) 
 
 Gastritis 
 
 Gastritis (Gr 2) 
 
 Gastroesophageal 
reflux disease 
 
  
 
 
Gastrointestinal 
perforation2 
  
Mucositis oral 
 
 
 Mucositis oral (Gr 3) 
Nausea 
 
 
 Nausea (Gr 3) 
 
Oral pain 
 
 Oral pain (Gr 2) 
 
 
Pancreatitis 
  
Rectal mucositis 
 
 
 Rectal mucositis (Gr 2) 
Small intestinal 
mucositis 
 
 
 Small intestinal mucositis 
(Gr 2) 
Vomiting 
 
 
 Vomiting (Gr 3) 
GENERAL DISORDERS AND ADMINISTRATION SITE CONDITIONS 
  
 
Chills 
 
 Chills (Gr 2) 
 
Edema limbs 
 
 Edema limbs (Gr 2) 
Fatigue 
 
 
 Fatigue (Gr 3) 
 
Fever 
 
 Fever (Gr 2)  
 
Flu like symptoms 
 
  
 
Non-cardiac chest pain  
 Non-cardiac chest pain  
(Gr 2) 
HEPATOBILIARY DISORDERS 
  
 
 
Cholecystitis 
  
 
 
Hepatic failure 
  
IMMUNE SYSTEM DISORDERS 
  
 
 
Allergic reaction3 
  
INFECTIONS AND INFESTATIONS 
  
 
 
Infections and infestations 
- Other (necrotizing 
fasciitis) 
  
INJURY, POISONING AND PROCEDURAL COMPLICATIONS 
  
 
 
Wound complication 
  

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Adverse Events with Possible 
Relationship to Sunitinib malate (SU011248 L-malate) 
(CTCAE 5.0 Term) 
[n= 7115] 
 
 
Specific Protocol 
Exceptions to Expedited 
Reporting (SPEER) 
Likely (>20%) 
Less Likely (<=20%) 
Rare but Serious (<3%)   
INVESTIGATIONS 
  
 
Alanine 
aminotransferase 
increased 
 
 Alanine aminotransferase 
increased (Gr 3) 
 
Alkaline phosphatase 
increased 
 
 Alkaline phosphatase 
increased (Gr 2) 
 
Aspartate 
aminotransferase 
increased 
 
 
Aspartate 
aminotransferase 
increased (Gr 3) 
 
Blood bilirubin 
increased 
 
 Blood bilirubin increased 
(Gr 2) 
 
CPK increased 
 
  
 
Creatinine increased 
 
 Creatinine increased (Gr 3) 
 
 
Electrocardiogram QT 
corrected interval 
prolonged 
  
 
Lipase increased 
 
 Lipase increased (Gr 4) 
 
Lymphocyte count 
decreased 
 
 Lymphocyte count 
decreased (Gr 2) 
 
Neutrophil count 
decreased 
 
 Neutrophil count 
decreased (Gr 4) 
 
Platelet count 
decreased 
 
 Platelet count decreased 
(Gr 4) 
 
Serum amylase 
increased 
 
 Serum amylase increased 
(Gr 2) 
 
Weight loss 
 
 Weight loss (Gr 2) 
 
White blood cell 
decreased 
 
 White blood cell decreased 
(Gr 3) 
METABOLISM AND NUTRITION DISORDERS 
  
Anorexia 
 
 
 Anorexia (Gr 3) 
 
Dehydration 
 
 Dehydration (Gr 3) 
 
Hyperuricemia 
 
 Hyperuricemia (Gr 2) 
 
Hypoalbuminemia 
 
 Hypoalbuminemia (Gr 2) 
 
Hypocalcemia 
 
  
 
 
Hypoglycemia 
  
 
Hypophosphatemia 
 
 Hypophosphatemia (Gr 2) 
 
 
Tumor lysis syndrome 
  
MUSCULOSKELETAL AND CONNECTIVE TISSUE DISORDERS 
  
 
Arthralgia 
 
 Arthralgia (Gr 2) 
 
Back pain 
 
 Back pain (Gr 2) 
 
 
Musculoskeletal and 
connective tissue disorder 
- Other (fistula formation) 
  
 
Myalgia 
 
 Myalgia (Gr 2) 
 
 
Osteonecrosis of jaw 
  

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Adverse Events with Possible 
Relationship to Sunitinib malate (SU011248 L-malate) 
(CTCAE 5.0 Term) 
[n= 7115] 
 
 
Specific Protocol 
Exceptions to Expedited 
Reporting (SPEER) 
Likely (>20%) 
Less Likely (<=20%) 
Rare but Serious (<3%)   
 
Pain in extremity 
 
 Pain in extremity (Gr 2) 
 
 
Rhabdomyolysis 
  
NEOPLASMS BENIGN, MALIGNANT AND UNSPECIFIED (INCL CYSTS 
AND POLYPS) 
  
 
 
Leukemia secondary to 
oncology chemotherapy 
  
 
 
Myelodysplastic syndrome   
NERVOUS SYSTEM DISORDERS 
  
 
Dizziness 
 
  
Dysgeusia 
 
 
 Dysgeusia (Gr 2) 
 
Headache 
 
 Headache (Gr 3) 
 
 
Leukoencephalopathy 
  
 
 
Nervous system disorders 
- Other (cerebral infarction)   
 
Paresthesia 
 
  
 
 
Reversible posterior 
leukoencephalopathy 
syndrome 
  
 
 
Transient ischemic attacks   
PSYCHIATRIC DISORDERS 
  
 
Depression 
 
  
 
Insomnia 
 
 Insomnia (Gr 2) 
RENAL AND URINARY DISORDERS 
  
 
 
Acute kidney injury 
  
 
 
Nephrotic syndrome 
  
 
 
Proteinuria 
  
RESPIRATORY, THORACIC AND MEDIASTINAL DISORDERS 
  
 
Cough 
 
 Cough (Gr 2) 
 
Dyspnea 
 
 Dyspnea (Gr 3) 
 
Epistaxis 
 
 Epistaxis (Gr 2) 
Laryngeal mucositis 
 
 
 Laryngeal mucositis (Gr 2) 
Pharyngeal 
mucositis 
 
 
 Pharyngeal mucositis  
(Gr 2) 
Tracheal mucositis 
 
 
 Tracheal mucositis (Gr 2)  
SKIN AND SUBCUTANEOUS TISSUE DISORDERS 
  
 
Alopecia 
 
 Alopecia (Gr 2) 
 
Dry skin 
 
 Dry skin (Gr 2) 
 
 
Erythema multiforme 
  
 
 Hair color changes 
 
 Hair color changes (Gr 2) 
Palmar-plantar 
erythrodysesthesia 
syndrome 
 
 
 
Palmar-plantar 
erythrodysesthesia 
syndrome (Gr 3) 
 
Pruritus 
 
  
 
Rash maculo-papular 
 
 Rash maculo-papular (Gr 3) 

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Adverse Events with Possible 
Relationship to Sunitinib malate (SU011248 L-malate) 
(CTCAE 5.0 Term) 
[n= 7115] 
 
 
Specific Protocol 
Exceptions to Expedited 
Reporting (SPEER) 
Likely (>20%) 
Less Likely (<=20%) 
Rare but Serious (<3%)   
 
 
Skin and subcutaneous 
tissue disorders - Other 
(pyoderma gangrenosum) 
  
 
Skin hypopigmentation 
 
 Skin hypopigmentation  
(Gr 2) 
 
 
Stevens-Johnson 
syndrome 
  
 
 
Toxic epidermal necrolysis   
VASCULAR DISORDERS 
  
 
Hypertension 
 
 Hypertension (Gr 3) 
 
 
Thromboembolic event 
  
 
Vascular disorders - 
Other (hemorrhage)4 
 
  
1 This table will be updated as the toxicity profile of the agent is revised.  Updates will be distributed to all 
Principal Investigators at the time of revision.  The current version can be obtained by contacting 
PIO@CTEP.NCI.NIH.GOV.  Your name, the name of the investigator, the protocol and the agent should 
be included in the e-mail. 
2 Gastrointestinal perforation includes Colonic perforation, Duodenal perforation, Esophageal perforation, 
Gastric perforation, Ileal perforation, Jejunal perforation, Rectal perforation, and Small intestinal 
perforation under the GASTROINTESTINAL DISORDERS SOC. 
3 Allergic reactions observed include anaphylaxis and angioedema. 
4 The majority of hemorrhage events were mild.  Major events, defined as symptomatic bleeding in a 
critical area or organ (e.g., eye, GI tract, GU system, respiratory tract, nervous system [including fatal 
intracranial hemorrhage, and cerebrovascular accident], and tumor site) have been reported. 
Adverse events reported on Sunitinib malate (SU011248 L-malate) trials, but for which 
there is insufficient evidence to suggest that there was a reasonable possibility that 
Sunitinib malate (SU011248 L-malate) caused the adverse event: 
BLOOD AND LYMPHATIC SYSTEM DISORDERS - Febrile neutropenia 
CARDIAC DISORDERS - Atrial fibrillation; Cardiac arrest; Pericardial effusion 
GASTROINTESTINAL DISORDERS - Ascites; Dysphagia; Gastrointestinal disorders - Other 
(enteritis); Hemorrhoids; Ileus; Small intestinal obstruction 
GENERAL DISORDERS AND ADMINISTRATION SITE CONDITIONS - Pain 
INVESTIGATIONS - GGT increased; INR increased 
METABOLISM AND NUTRITION DISORDERS - Hypercalcemia; Hyperglycemia; 
Hyperkalemia; Hypokalemia; Hyponatremia 
MUSCULOSKELETAL AND CONNECTIVE TISSUE DISORDERS - Bone pain 
NERVOUS SYSTEM DISORDERS - Cognitive disturbance; Peripheral sensory neuropathy; 
Seizure; Spinal cord compression; Syncope 
PSYCHIATRIC DISORDERS - Anxiety; Confusion 
RENAL AND URINARY DISORDERS - Hematuria; Urinary retention 
REPRODUCTIVE SYSTEM AND BREAST DISORDERS - Hematosalpinx 

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EAY131-V 
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NCI Update Date: August 12, 2015 
26 
RESPIRATORY, THORACIC AND MEDIASTINAL DISORDERS - Pharyngolaryngeal pain; 
Pleural effusion; Pneumothorax 
VASCULAR DISORDERS - Flushing; Hypotension 
NOTE: 
Sunitinib malate (SU011248 L-malate) in combination with other agents could cause 
an exacerbation of any adverse event currently known to be caused by the other 
agent, or the combination may result in events never previously associated with 
either agent. 
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3.4 
Dose Modifications 
All toxicity grades below are described using the NCI Common Terminology 
Criteria for Adverse Events (CTCAE) version 4.0. 
All appropriate treatment areas should have access to a copy of the CTCAE 
version 4.0. A copy of the CTCAE version 4.0 can be downloaded from the 
CTEP website (http://ctep.cancer.gov). 
Dose interruption and/or dose modification in 12.5 mg increments or decrements 
is recommended based on individual safety and tolerability. 
The acceptable dose levels for sunitinib therapy are listed below in the following 
table.  Treatment is initiated at dose level 0, if a dose reduction occurs for grade 
II or III toxicity, and a patient tolerates the dose reduction well, and is deriving 
clinical benefit, a dose level escalation back to the prior dose may be considered 
after 1 cycle.   
Dose Level 
Dose and Administration Schedule 
0 
50mg po daily for 4 weeks, 2 weeks rest 
-1 
37.5 mg po daily for 4 weeks, 2 weeks rest 
-2 
25 mg po daily for 4 weeks, 2 weeks rest 
-3 
Discontinue therapy 
If the drug is held longer than 2 weeks (excluding 2 week rest period), 
discontinue sunitinib. 
Specific dose modification criteria and management in response to specific 
toxicities are listed in the table below: 

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NCI Update Date: August 12, 2015 
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Table 1. Sunitinib Dose-Reduction Guidelines  
Toxicity 
Sunitinib Modification 
Skin and Subcutaneous Disorders 
Palmar-plantar 
erythrodysesthesia syndrome 
(PPE) (hand-foot syndrome) 
See table 2 below ‘Sunitinib Dose Reductions for PPE (Hand-Foot 
Syndrome)’ 
Grade 3 or 4 
rash acneiform 
Hold sunitinib 
x Re-evaluate at least weekly until resolution to ≤ grade 1 or 
tolerable grade 2 
x Re-start sunitinib at one dose-reduction step 
x If AE persists > 14 days, discontinue sunitinib 
x If grade 4 acneiform rash (related to sunitinib), sunitinib may be 
discontinued at investigator’s discretion 
Stevens-Johnson syndrome or 
toxic epidermal necrolysis 
Discontinue sunitinib if Stevens-Johnson syndrome or toxic 
epidermal necrolysis are suspected 
Gastrointestinal Disorders 
Perforation (esophageal, 
gastric, colonic, duodenal, ileal, 
jejunal, rectal, or small intestine) 
Discontinue sunitinib 
Investigations 
Grade 3 or 4  
AST or ALT increase 
Hold sunitinib 
x If no alternative explanation for transaminitis can be determined 
(such as viral hepatitis, progressive underlying hepatic 
malignancy), discontinue sunitinib 
x Otherwise, upon resolution to ≤ grade 1 or baseline, re-start 
sunitinib at one dose-reduction step 
x If patient develops ≥ grade 3 hepatic failure, discontinue 
sunitinib. 
Grade 3 or 4 electrocardiogram 
QT corrected interval prolonged  
See also Section 3.5.4. Hold sunitinib 
x Check and immediately administer potassium to achieve levels 
of ≥ 4  mmol/L and magnesium to levels of ≥ 2 mg/dL 
x Consider chronic oral supplementation of potassium and/or 
magnesium 
x Review with the subprotocol principal investigator and consult 
with a cardiologist prior to patient’s next scheduled treatment, 
considering the following options: 
- 
HOLD sunitinib until QTc recovers to pre-study treatment 
baseline (grade 1 or less, or ≤ 480ms) 
- 
When QTc returns to baseline, reinitiate sunitinib 
cautiously, with additional QTc monitoring at earliest 
possible follow-up opportunity, but no more than 8 days 
from reintroduction of sunitinib 
- 
If QTc prolongation event felt attributable to sunitinib, 
follow protocol dose-reduction-step guidelines (see table 
above in Section 3.4) when re-introduced 
- 
For recurrent QTc grade 3 felt attributable to sunitinib 
despite dose-step reduction, discontinue sunitinib 

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Proteinuria 
Monitor urine protein once every cycle with urinalysis.  If protein 
excretion positive on urinalysis, obtain 24-hour urine protein.  
 
Interrupt treatment for 24-hour urine protein ≥ 3 grams. 
Discontinue for repeat episodes of protein ≥ 3 grams despite dose 
reductions or nephrotic syndrome. 
Nervous System Disorders (potentially reflective of cardio-toxicity) 
Grade 2 pre-syncope or grade 3 
syncope 
See also Section 3.5.2. 
x 
Obtain ECG for cardiology review/consultation 
x 
Check magnesium and potassium and promptly administer 
potassium to achieve level of ≥ 4 mmol/L and magnesium to 
level ≥ 2 mg/dL 
x 
IF ECG shows new dysrhythmia or QTc ≥ grade 2 (> 480ms), 
hospitalize for monitoring with cardiology consultation  
x 
HOLD sunitinib until any potassium and magnesium 
abnormalities are corrected, symptoms resolved and QTc 
returns to grade 1 or less (≤ 480ms) 
x 
Reintroduce sunitinib cautiously, with input from cardiology 
and with additional QTc evaluation, either concurrent with 
reintroduction or at earliest possible follow-up opportunity and 
no more than 8 days from reintroduction 
x 
If event felt attributable to sunitinib consider dose modification 
of sunitinib when re-introduced 
x 
Consider chronic oral supplementation of potassium and/or 
magnesium 
x 
For recurrent syncope or near-syncope felt attributable to 
sunitinib consider permanent discontinuation 
All Other Non-Hematologic Toxicities Attributable to sunitinib 
Any grade 2 non-hematologic 
toxicity that is persistent, 
intolerable, or unresponsive to 
optimal management  
At the treating investigator’s discretion, reduce to the next lower 
dose-reduction step  
Grade 3 or 4 
Omit sunitinib until resolution to ≤ grade 1, baseline or tolerable 
grade 2 
x 
Re-start sunitinib at one dose-reduction step 
x 
If AE persists > 14 days, discontinue sunitinib 
 
In addition, at investigator discretion: 
x 
For bleeding that requires more than minor medical 
intervention, consider discontinuing sunitinib 
x 
For severe persistent hypertension or hypertensive crisis 
despite optimal antihypertensive management, consider 
discontinuing sunitinib 
x 
For evidence of cardiac ischemia or myocardial infarction, 
consider discontinuing sunitinib 
x 
For grade 4 AEs related to sunitinib, consider discontinuing 
sunitinib 

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Dose reduction guideline table for Plantar Palmar Erythrodysesthesia 
Table 2. Sunitinib Dose-Reduction Guidelines and Management for PPE 
Grade 
Occurrence 
Action 
Grade 1 
1st occurrence or 
recurrence 
Continue sunitinib and institute 
supportive measures for 
symptomatic relief.* 
Grade 2: Moderate and painful skin 
changes of hands and/or feet such 
as peeling, blisters, bleeding, 
hyperkeratosis, erythema, swelling; 
and/or any such changes that are 
limiting instrumental activities of daily 
living (preparing meals, shopping for 
groceries, using the telephone, 
managing money, etc) 
1st or 2nd occurrence 
Continue sunitinib and institute 
supportive measures for 
symptomatic relief.* If no 
improvement within 7 days, see 
below. 
No improvement 
within 7 days or 
recurrence beyond 2nd 
occurrence 
Stop sunitinib treatment until toxicity 
resolves to grade 0-1. When 
resuming treatment, decrease 
sunitinib dose by 1 dose-reduction 
step.  
Institute supportive measures for 
symptomatic relief.* 
Grade 3: Severe and painful skin 
changes of the hands and/or feet, 
such as moist desquamation, 
ulceration, blistering, bleeding, 
hyperkeratosis, erythema, swelling; 
and/or any such severe changes or 
pain that are limiting self-care 
activities of daily living (bathing, 
dressing, feeding self, using toilet, 
taking medications or becoming 
bedridden) 
1st or 2nd occurrence 
Stop sunitinib treatment until toxicity 
resolves to grade 0-1. When 
resuming treatment, decrease s 
sunitinib by 1 dose-reduction step. 
Institute supportive measures for 
symptomatic relief.* 
3rd occurrence 
Discontinue sunitinib treatment. 
* See section 3.5.3 for PPE management 
Table 3. Other Hematologic and Non-Hematologic Adverse Events 
Event 
AE Grade or Observation 
Dose modification 
Neutropenia 
Grades 1 and 2 
Maintain dose 
Grade 3* 
Hold sunitinib until ≤ grade 2, then resume at same 
dose  level 
Grade 4 
Hold sunitinib until ≤ grade 2, then reduce 1 dose 
level and resume treatment 
Thrombocytopenia 
Grades 1 and 2 
Maintain dose 
Grade 3* and severe 
grade 2, at investigator 
discretion 
Hold sunitinib until ≤ grade 2, then reduce 1 dose 
level and resume treatment 
Grade 4 
Hold sunitinib until ≤ grade 2, then reduce 1 dose 
level and resume treatment 
* Recurrent grade 3 events require dose reduction. 

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NCI Update Date: August 12, 2015 
31 
3.5 
General Concomitant Medications & Supportive Care Guidelines 
3.5.1 
All supportive measures consistent with optimal patient care will be 
given throughout the study.  
3.5.2 
Hypertension  
3.5.2.1 
Hypertension is common during sunitinib therapy. Patients 
should be monitored for hypertension and treated as 
needed with standard anti-hypertensive therapy. In cases 
of severe or symptomatic hypertension, temporary 
suspension of sunitinib is recommended until hypertension 
is controlled.  If hypertension is associated with neurologic 
or cardiac symptoms, institute dose reduction or consider 
discontinuation as per table 1, in Section 3.4 
3.5.3 
Plantar Palmar Erythrodysesthesia (PPE) 
Biopsy specimens of patients with PPE secondary to tyrosine kinase 
inhibition show hyperkeratosis, keratinocyte necrosis, and dermal 
inflammation. Recommended management strategies for skin 
toxicities consistent with PPE are summarized in the following 
sections: 
3.5.3.1 
PPE Prevention 
x 
Before initiating treatment with sunitinib, check the 
condition of the patient’s hands and feet. Suggest a 
manicure/pedicure, when indicated. Recommend use 
of a pumice stone for callus or rough spot removal.  
x 
During sunitinib treatment, instruct patients to avoid 
pressure points and items that rub, pinch, or create 
friction. 
x 
Instruct the patient to apply moisturizing lotions to their 
hands and feet twice a day throughout treatment. 
3.5.3.2 
PPE Treatment 
x 
Treatment may begin at the first clinical signs of PPE.  
At first occurrence, independent of grade, supportive 
measures should be promptly initiated. Tender areas 
should be protected as follows: 
x 
Use socks/gloves to cover moisturizing creams 
x 
Wear well-padded footwear; use insole cushions or 
inserts. 
x 
Foot soaks with tepid water and Epson salts. 
x 
Creams may be used as follows: 
x 
Non-urea based creams may be applied liberally.  
x 
Keratolytic creams (eg, urea-based creams, salicylic 
acid 6%) may be used sparingly and only to affected 
hyperkeratotic areas.  

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NCI Update Date: August 12, 2015 
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x 
Alpha hydroxyl acids (AHA)-based creams may be 
applied liberally 2 times a day. Approximately 5% to 
8% provides gentle chemical exfoliation.  
x 
Topical analgesics (eg, lidocaine 2%) may be used for 
pain control.  
x 
Topical corticosteroids like clobetasol 0.05% should be 
considered for patients with grade 2 or 3 PPE. 
Systemic steroids should be avoided. 
x 
Use of celecoxib: A meta-analysis of PPE prevention 
strategies concluded that celecoxib, with statistically 
significant results, was the most promising agent. 
Therefore, celecoxib can be considered to reduce the 
severity of PPE as follows: Celecoxib 200 mg once 
daily should begin at the first clinical signs or 
symptoms of grade 2 or greater PPE. 
3.5.4 
QT Prolongation Considerations During Therapy 
3.5.4.1 
Any time QTc is evaluated:  
x 
When HR is between 60-100 bpm, no manual read of 
QTc required 
x 
When HR < 60 or >100 bpm, manual read of QTc by 
member of the study team is required, using Fridericia 
correction  
3.5.4.2 
To the extent possible, concurrent use of sunitinib with 
drugs known to cause clinically significant QT prolongation 
should be avoided. Such drugs may be identified with 
reference to Appendix III in the subprotocol, in addition to 
the Credible Meds website (http://crediblemeds.org/login). 
The Credible Meds website requires free user registration 
to view the list of clinically relevant QT prolonging drugs, 
eg, those known to carry a risk of causing Torsade de 
Pointes. QT prolonging drugs to be avoided during this trial 
are shown in the Credible Meds list of “drugs with known 
TdP risk.”   
3.5.4.3 
When concurrent use of sunitinib with any drug on the 
Credible Meds list of “drugs with known TdP risk” cannot 
be avoided, review QTc prior to concurrent use. If pre-
concurrent use QTc is: 
x 
Grade 0 (< 450 ms), follow-up QTc evaluation should 
be done at the next scheduled follow-up visit. 
x 
Grade 1 (450-480 ms), follow-up QTc evaluation 
should be done within 8 days after concurrent use 
starts. 
x 
Grade 2 (481-500 ms), withhold study drug until follow-
up ECG at next possible opportunity shows QTc ≤ 
grade 1 (≤ 480 ms); evaluate QTc within 8 days after 
reintroduction of study drug. 

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NCI Update Date: August 12, 2015 
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3.5.4.4 
Any new onset of dysrhythmia on ECG during therapy will 
be reviewed and managed with input from cardiology. 
3.5.4.5 
For any episode of syncope (grade 3) or near-syncope 
(pre-syncope grade 2) or QTc grade 3 or 4 (> 500 ms on 2 
ECGs), see Table 1 in section 3.4 
3.5.5 
Hypothyroidism 
3.5.5.1 
Sunitinib is associated with thyroid dysfunction. Monitor 
thyroid function once every cycle, and as part of 
investigations for fatigue or tremor. Thyroid dysfunction 
should be managed as part of routine standard of care. 
3.6 
Duration of Agent-specific treatment  
In the absence of treatment delays due to adverse event(s), treatment may 
continue until one of the following criteria applies: 
x 
Extraordinary Medical Circumstances: If at any time the constraints of this 
protocol are detrimental to the patient's health, protocol treatment should be 
discontinued. In this event submit forms according to the instructions in the 
MATCH Forms Packet. 
x 
Patient withdraws consent. 
x 
Patient experiences unacceptable toxicity. 
x 
Non-protocol therapies are administered. 
x 
Disease progression 
3.7 
Duration of Follow-Up 
Refer to the MATCH Master Protocol for specifics on the duration of follow-up. 

ECOG-ACRIN 
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NCI Update Date: August 12, 2015 
34 
4. 
Study Parameters 
4.1 
Therapeutic Parameters for Sunitinib Treatment  
NOTE: 
In addition to the study parameters listed in the MATCH Master Protocol, the below parameters must also be 
performed for patients receiving sunitinib treatment.  
NOTE: 
All assessments required prior to registration to treatment should be done ≤ 4 weeks prior to registration to 
Steps 1, 3, 5, 7, excluding the radiologic evaluation and electrocardiogram (ECG). 
Test/Assessment 
Prior to 
Registration 
to Treatment 
Treatment 
End of 
Treatment 
Follow 
UpF 
Every Cycle, 
prior to 
treatment 
For Cycle 
1, Week 1-
4 and 6 
For Cycles 1 
and 2, Day 21 
(± 3 days)O 
Every 2 
Cycles 
H&P, Weight, Vital signsA 
X 
 XJ 
XA 
X 
 
 
X 
Performance status 
X 
 XJ 
 
 
 
 
X 
CBC w/diff, pltsB 
X 
 XJ 
 
X 
 
 
X 
Serum chemistryB 
X 
 XJ 
 
X 
 
 
X 
Radiologic evaluationD 
X 
 
 
 
 XD 
 
 XF 
E-HCGC 
X 
 
 
 
 
 
 
Urinalysis for proteinuriaL 
X 
X 
 
X 
 
 
 
Thyroid function testsM 
X 
X 
 
X 
 
 
 
Echocardiogram or Nuclear StudyN 
XI 
 
 
 
XI 
 
 
Toxicity AssessmentG 
 
X 
 
 
 
X 
 XF 
Pill Count/DiaryH 
 
X 
 
 
 
X 
 
ECGK 
X 
 XI 
 
 
 
 
 
Tumor biopsy and blood sample submission for MATCH Master ProtocolE 
 
 
 
 
X 
X 
 
A. History and physical, including vital signs and weight at the start of each cycle (up to 3 days before start of new cycle). During Cycle 1, blood 
pressure will be monitored weekly (except for week 5). 
B. Albumin, alkaline phosphatase, total bilirubin, bicarbonate, BUN, calcium, creatinine, glucose, phosphorus, potassium, SGOT[AST], SGPT[ALT], 
sodium, magnesium and serum tumor markers (including LDH, PSA if appropriate).  For eligibility purposes, participants with creatinine levels 
above institutional normal, Cockcroft-Gault will be used to calculate creatinine clearance. CBC w/diff, platelets and serum chemistries should be 
performed on cycle 1, day 1 (or up to 7 days prior), and at the start of each subsequent cycle (up to 3 days before start of new cycle). CBC with 
differential will be performed more frequently in patients with grade 4 neutropenia or thrombocytopenia until resolution to ≤ grade 3. CBC and 
serum chemistries are only required in follow-up until values return to pre-treatment levels or until progressive disease. 
C. Blood pregnancy test (women of childbearing potential) required prior to beginning treatment. 
Rev.2/16 
Rev.2/16 
Rev.2/16 
Rev.12/16, 
Add13 
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D. Disease measurements are repeated every 2 cycles until PD or start of another MATCH treatment step. The baseline evaluation should be 
performed as closely as possible to the beginning of treatment and never more than 6 weeks before registration to treatment step. For multiple 
myeloma patients, please refer to Section 6.4 of the MATCH Master Protocol for additional information on myeloma response criteria and the 
required disease assessments. Documentation (radiologic) must be provided for patients removed from study for progressive disease. 
E. Additional blood specimens and/or biopsies are to be submitted from consenting patients per Section 9.3.2 of the MATCH Master Protocol. Submit 
at the following time points, as applicable: 
x 
Blood specimens are to be submitted at the end of Cycle 2 (prior to start of Cycle 3 treatment). If patient progresses or treatment is 
discontinued prior to Cycle 3, collect the blood at that time instead. On-treatment kits for blood sample collections will be automatically shipped 
to sites upon registration to the treatment step. 
x 
Screening biopsies for additional aMOI assessments after registration to appropriate screening step, if applicable (Step 2 or Step 4). 
x 
At end of all MATCH study treatments, blood specimens and/or research biopsy after consent and registration to Step 8 
Please refer to Section 4 of the MATCH Master Protocol to determine whether the patient proceeds to the next screening step or to follow-up (with 
a potential end of treatment biopsy for research purposes on Step 8). Samples are to be submitted as outlined in Section 9 of the MATCH Master 
Protocol. To order Step 2/4 Screening or Step 8 kits, complete the EAY131 Collection and Shipping Kit Order Form (See Appendix XII of the 
MATCH Master Protocol) and fax to 713-563-6506. 
F. Every 3 months if patient is < 2 years from study entry, and every 6 months for year 3. Toxicity assessments and radiologic evaluations are not 
required to be done during Follow Up if progression has been previously reported; however if an adverse event occurs post treatment that meets 
the SAE reporting requirements, it still must be reported via CTEP-AERS, even if progression has occurred. 
G. Site personnel should evaluate for toxicity and discuss treatment compliance with the patient in order to ensure the medication is taken correctly; 
this evaluation may be conducted by telephone or in person. The Toxicity Assessment is not required prior to Cycle 1, but is required every 
subsequent cycle. 
H. The pill calendar will be collected at the end of every cycle. The Pill Count/Diary is not required prior to Cycle 1, but is required every subsequent 
cycle. 
I. As clinically indicated. 
J. For Cycle 1, if the following tests/assessments occurred within 7 days of Day 1, they do not need to be repeated at this timepoint: H&P, Weight, 
Vital Signs; Performance Status; CBC w/diff, plts; Serum chemistry; Concomitant Medications. 
K. Within 8 weeks of treatment assignment. 
L. If urinalysis is positive for protein excretion, obtain 24 hour urine protein. 
M. TSH, T3, T4  
N. Cardiac monitoring with echocardiogram or nuclear study (MUGA/First Pass) must be completed within 4 weeks prior to registration to treatment, if 
clinically indicated, and then repeated every 2 cycles thereafter, if clinically indicated. 
O. For Cycles 1 and 2, an additional visit for toxicity testing will be done mid-cycle (within 3 days of Day 21) to detect any toxicities before the 2 
weeks of rest. 
 
Rev.2/16 
Rev.2/16 
Rev.10/15 
Rev.2/16 

ECOG-ACRIN 
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36 
5. 
Drug Formulation and Procurement 
This information has been prepared by the ECOG-ACRIN Pharmacy and Nursing 
Committees. 
Availability 
NO STARTER SUPPLIES MAY BE ORDERED. Subjects must be enrolled and assigned 
to the treatment subprotocol prior to submitting the clinical drug request to PMB. 
Drug Ordering: NCI supplied agents may be requested by the eligible participating 
Investigators (or their authorized designee) at each participating institution. 
Pharmaceutical Management Branch (PMB) policy requires that drug be shipped directly 
to the institution where the patient is to be treated. PMB does not permit the transfer of 
agents between institutions (unless prior approval from PMB is obtained – see general 
information) The CTEP-assigned protocol number must be used for ordering all CTEP-
supplied investigational agents. The eligible participating investigators at each 
participating institution must be registered with CTEP, DCTD through an annual 
submission of FDA Form 1572 (Statement of Investigator), NCI Biosketch, Agent 
Shipment Form, and Financial Disclosure Form (FDF). If there are several participating 
investigators at one institution, CTEP-supplied investigational agents for the study 
should be ordered under the name of one lead investigator at that institution. 
Submit agent requests through the PMB Online Agent Order Processing (OAOP) 
application (https://ctepcore.nci.nih.gov/OAOP). Access to OAOP requires the 
establishment of a CTEP Identity and Access Management (IAM) account 
(https://ctepcore.nci.nih.gov/iam) and the maintenance of an “active” account status, a 
“current” password, and an active person registration status. 
NCI Supplied Agent(s) – General Information 
Questions about drug orders, transfers, returns, or accountability should be 
addressed to the PMB by calling 240-276-6575 Monday through Friday between 
8:30 AM and 4:30 PM Eastern Time or email PMBAfterHours@mail.nih.gov 
anytime. 
Drug Returns: All undispensed drug supplies should be returned to the PMB. When it is 
necessary to return study drug (e.g., sealed bottles remaining when PMB sends a stock 
recovery letter), investigators should return the study drug to the PMB using the NCI 
Return Agent Form available on the NCI home page (http://ctep.cancer.gov).  
Drug Accountability: The investigator, or a responsible party designated by the 
investigator, must maintain a careful record of the receipt, disposition, and return of 
agent received from the PMB using the NCI Investigational Agent Accountability Record 
Form for Oral Agents available on the NCI home page (http://ctep.cancer.gov). Maintain 
separate NCI Investigational Agent Accountability Records for each agent, strength, 
formulation and ordering investigator. 
Investigator Brochure Availability: The current versions of the IBs for PMB-supplied 
agents will be accessible to site investigators and research staff through the PMB Online 
Agent Order Processing (OAOP) application. Access to OAOP requires the 
establishment of a CTEP Identity and Access Management (IAM) account and the 
maintenance of an “active” account status, a “current” password, and active person 
registration status. Questions about IB access may be directed to the PMB IB 
coordinator at IBCoordinator@mail.nih.gov 
Rev.12/16 
Rev.3/17 
Rev. Add13 

ECOG-ACRIN 
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NCI Update Date: August 12, 2015 
37 
5.1 
Sunitinib malate (NSC 736511) 
5.1.1 
Chemical Name: 
N-[2-(Diethylamino)ethyl]-5-[(Z)-(5-fluoro-1,2-dihydro-2-oxo-3H-indol-
3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-carboxamide, compound 
with (S)-2-hydroxybutanedioic acid 
5.1.2 
Other Names:  
SU011248 L-Malate, Sutent 
5.1.3 
Classification: 
Multi-kinase inhibitor 
5.1.4 
Molecular Formula: 
C22H27FN4O2•C4H6O5 
5.1.5 
Physical Description: 
Yellow to orange powder 
5.1.6 
CAS Registry Number: 
341031-54-7 
5.1.7 
Solubility: 
Aqueous Solubility 
Solvent 
Solubility (mg/mL) 
0.1 M HCl 
59.1  
pH 4.5 buffer 
25.4  
pH 6.8 buffer 
37.8 
pH 7.5 buffer 
0.05  
In Water  
1.6 
Solubility in Various Solvents 
Solvent 
Solubility (mg/mL) 
Acetonitrile 
0.1 
Dimethyl sulfoxide 
92.9 
Tetrahydrofuran 
0.2 
Methanol 
1.5 
Ethanol 
0.3 
1-Butanol 
0.1 
1-Butano:Water (80/20 v/v) 
6.2 
N,N-Dimethylacetamide 
37 
N,N-Dimethylformamide 
18.4 
5.1.8 
Mode of Action: 
Sunitinib is a small molecule that inhibits multiple receptor tyrosine 
kinases (RTKs), some of which are implicated in tumor growth, 

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38 
pathologic angiogenesis, and metastatic progression of cancer. 
Sunitinib is an inhibitor of platelet-derived growth factor receptors 
(PDGFRα and PDGFRβ), vascular endothelial growth factor receptors 
(VEGFR1, VEGFR2 and VEGFR3), stem cell factor receptor (KIT), 
Fms-like tyrosine kinase-3 (FLT3), colony stimulating factor receptor 
Type 1 (CSF-1R), and the glial cell-line derived neurotrophic factor 
receptor (RET). 
5.1.9 
Storage and Stability:  
Storage: 
Store at 25°C (77°F); excursions permitted to 15–30°C 
(59–86°F). 
Stability: 
Refer to the package label for expiration. 
5.1.10 
Dose Specifics:  
50 mg po once a day for 4 weeks, followed by 2 weeks rest. 
5.1.11 
Preparation:  
Sunitinib malate capsules are supplied by Pfizer, Inc. and distributed 
by the Pharmaceutical Management Branch, CTEP/DCTD/NCI.  
Capsules are packaged in 28-count bottles with mannitol, 
croscarmellose sodium, povidone (K-25) and magnesium stearate as 
inactive ingredients in the following strengths: 
x 
12.5 mg hard gelatin capsule (size 4) with orange cap and orange 
body, printed with white ink "Pfizer" on the cap and "STN 12.5 mg" 
on the body.  
x 
25 mg hard gelatin capsule (size 3) with caramel cap and orange 
body, printed with white ink "Pfizer" on the cap and "STN 25 mg" 
on the body.  
x 
50 mg hard gelatin capsule (size 2) with caramel top and caramel 
body, printed with white ink "Pfizer" on the cap and "STN 50 mg" 
on the body.  
Orange gelatin capsule shells contain titanium dioxide, and red iron 
oxide. Caramel gelatin capsule shells contain titanium dioxide, red 
iron oxide, yellow iron oxide and black iron oxide.  White printing ink 
contains shellac, propylene glycol, sodium hydroxide, povidone and 
titanium dioxide.  
5.1.12 
Route of Administration:  
Oral administration, take with or without food. 
5.1.13 
Potential Drug Interactions: 
Sunitinib is metabolized primarily by CYP3A4. Avoid coadministration 
of strong CYP3A4 inducers/inhibitors. 
5.1.14 
Side Effects:  
See Section 3.3 for side effects. 

ECOG-ACRIN 
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39 
6. 
Translational Studies 
Please refer to the MATCH Master Protocol for information on the Translational Studies.  
7. 
References 
1. O'Farrell, A.M., T.J. Abrams, H.A. Yuen, et al.  (2003a).  SU11248 is a novel FLT3 
tyrosine kinase inhibitor with potent activity in vitro and in vivo.  Blood.  101:3597-
3605. 
2. Chow, L.Q., and S.G. Eckhardt.  (2007).  Sunitinib: from rational design to clinical 
efficacy.  J Clin Oncol.  25:884-896. 
3. Faivre, S, G. Demetri, W. Sargent, E. Raymond (2007). Molecular basis for sunitinib 
efficacy and future clinical development.  Nat Rev Drug Discov. 6:734-745. 
4. Gan, H.K., B. Seruga, and J.J. Knox.  (2009). Sunitinib in solid tumors.  Expert Opin 
Investig Drugs.  18:821-834. 
5. Mashkani, B., R. Griffith, and L.K. Ashman.  (2010). Colony stimulating factor-1 
receptor as a target for small molecule inhibitors.  Bioorg Med Chem.  18:1789-1798. 
6. Mendel, D.B., A. Douglas Laird, X. Xin, et al.  (2003). In vivo antitumor activity of 
SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth 
factor and platelet-derived growth factor receptors:  Determination of a 
pharmacokinetic/pharmacodynamic relationship.  Clin Cancer Res.  9:327-337. 
7. Goodman, V. L., E.P. Rock, R. Dagher, et al.  (2007). Approval summary: sunitinib 
for the treatment of imatinib refractory or intolerant gastrointestinal stromal tumors 
and advanced renal cell carcinoma.  Clin Cancer Res.  13:1367-1373. 
8. Izzedine, H., I. Buhaescu, O. Rixe, and G. Deray.  (2007).  Sunitinib Malate.  Cancer 
Chemother Pharmacol.  60:357-364. 
9. Rock, E.P., V. Goodman, J.X. Jiang, et al. (2007). Food and Drug Administration 
drug approval summary: Sunitinib malate for the treatment of gastrointestinal stromal 
tumor and advanced renal cell carcinoma.  Oncologist.  12:107-113 
10.  Hornick JL, Fletcher CD. The role of KIT in the management of patients with 
gastrointestinal stromal tumors. Hum Pathol 2007; 38: 679-687. 
11. Hoeben A, Schoffski P, Debiec-Rychter M. Clinical implications of mutational 
analysis in gastrointestinal stromal tumours. Br J Cancer 2008; 98: 684-688. 
12. Heinrich MC, Corless CL, Demetri GD, Blanke CD et al. Kinase mutations and 
imatinib response in patients with metastatic gastrointestinal stromal tumor. J Clin 
Oncol 2003; 21: 4342-9. 
13. Yavuz AS, Lipsky PE, Yavuz S et al. Evidence for the involvement of a 
hematopoietic progenitor cell in systemic mastocytosis from single-cell analysis of 
mutations in the c-kit gene. Blood 2002; 100: 661-5. 
14. Park SH, Chi HS, Min SK et al. Prognostic impact of c-kit mutations in core binding 
factor acute myeloid leukemia. Leuk Res 2011; 35: 1376-83. 
15. Kemmer K, Corless CL, Fletcher JA, et al. Kit mutations are common in testicular 
seminomas. Am J Pathol 2004; 164: 305-13. 

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Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
40 
16. Hoei-Hansen CE, Kraggerud SM, Abeler VM et al. Ovarian dysgerminomas are 
characterized by frequent kit mutations and abundant expression of pluripotency 
markers. Mol Cancer 2007; 6:12. 
17. Beadling C, Jacobson-Dunlop E, Hodi FS et al. Kit gene mutations and copy number 
in melanoma subtypes. Clin Cancer Res 2008; 14: 6821-8. 
18. Ashman LK, Griffith R. Therapeutic targeting of c-KIT in cancer. Expert Opin Invetig 
Drugs 2013; 22: 103-115. 
19. Cerami E, Gao J, Dogrusoz U, Gross BE et al. The cBio cancer genomics portal: an 
open platform for exploring multidimensional cancer genomics data. Cancer Discov 
2012; 2: 401-404. 
20. Investigator’s Brochure Sunitinib Malate (July 2014).  Pfizer, Inc. and Affiliates. 
21. Abrams, T.J., L.B. Lee, L.J. Murray, et al.  (2003a). SU11248 inhibits Kit and platelet-
derived growth factor receptor β in preclinical models of human small cell lung 
cancer.  Mol Cancer Therap.  2:471-478. 
22. Mendel, D.B., A. Douglas Laird, X. Xin, et al.  (2003). In vivo antitumor activity of 
SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth 
factor and platelet-derived growth factor receptors:  Determination of a 
pharmacokinetic/pharmacodynamic relationship.  Clin Cancer Res.  9:327-337. 
23. Abrams, T.J., L.J. Murray, E. Presenti, et al.  (2003b). Preclinical evaluation of the 
tyrosine kinase inhibitor SU11248 as a single agent and in combination with 
“standard of care” therapeutic agents for the treatment of breast cancer.  Mol Cancer 
Therap.  2:1011-1021. 
24. Sakamoto, K.M.  (2004)  Su-11248 Sugen. Curr Opin Invest Drugs.  5:1329-1339. 
25. Faivre, S., C. Delbaldo, K. Vera, et al. (2006). Safety, pharmacokinetic, and 
antitumor activity of SU11248, a novel oral multitarget tyrosine kinase inhibitor, in 
patients with cancer.  J Clin Oncol 24:25-35. 
26. Bello, C.L., L. Sherman, J. Zhou, et al.  (2006). Effect of food on the 
pharmacokinetics of sunitinib malate (SU11248), a multi-targeted receptor tyrosine 
kinase inhibitor:  Results from a phase I study in healthy subjects.  Anticancer Drugs.  
17:353-358. 
27. Fiedler, W., H. Serve, H. Döhner, et al.  (2005). A phase 1 study of SU11248 in the 
treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not 
amenable to conventional therapy for the disease.  Blood.  105:986-993. 
28. Washington, C., M. Eli, C. Bello, et al.  (2003). The effect of ketoconazole (KETO), a 
potent CYP3A4 inhibitor, on SU011248 pharmacokinetics (PK) in Caucasian and 
Asian healthy subjects.  ASCO Meeting Abstracts.  22:A553. 
29. Bello, C., B. Houk, L. Sherman, et al.  (2005). Effect of rifampin on the 
pharmacokinetics of SU11248 in healthy volunteers.  ASCO Meeting Abstracts.  
23:A3078. 
30. Britten, C.D., F. Kabbinavar, J.R. Hecht, et al.  (2008). A phase I and 
pharmacokinetic study of sunitinib administered daily for 2 weeks, followed by a 1-
week off period.  Cancer Chemother Pharmacol.  61:515-524. 
31. George, D.J., G. Liu, G. Wilding, et al.  (2008). Sunitinib in combination with 
docetaxel and prednisone in patients with metastatic hormone-refractory prostate 
cancer (mHRPC) - preliminary results.  ASCO Meeting Abstracts.  26:A5131. 

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Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
41 
32. Stadler, W.M.  (2006). New targets, therapies, and toxicities:  Lessons to be learned.  
J Clin Oncol.  24:4-5. 
33. Sutent Prescribing Information (December 2014). Pfizer Laboratories, Division of 
Pfizer Inc. <http://labeling.pfizer.com/ShowLabeling.aspx?id=607>. 
34. Robert, C., J.-C. Soria, A. Spatz, et al. (2005). Cutaneous side-effects of kinase 
inhibitors and blocking antibodies.  Lancet  6:491-500. 
35. Suwattee, R.  (2008). Sunitinib: A cause of bullous palmoplantar erythrodysesthesia, 
periungual erythema, and mucositis.  Arch Dermatol.  144:123-125. 
36. Porta, C., C. Paglino, I. Imarisio, and L. Bonomi.  (2007).  Uncovering Pandora's 
vase:  The growing problem of new toxicities from novel anticancer agents.  The 
case of sorafenib and sunitinib.  Clin Exp Med.  7:127-134. 
37. Rosenbaum, S.E., S. Wu, M.A. Newman, et al.  (2008). Dermatological reactions to 
the multitargeted tyrosine kinase inhibitor sunitinib.  Support Care Cancer.  
16(6):557-66. 
38. Shah RR, Morganrath J, Shah DR. Hepatotoxicity of tyrosine kinase inhibitors: 
clinical and regulatory perspectives. Drug Saf 2013; 36: 491-503. 
39. Chu, T.F., M.A. Rupnick, R. Kerkela, et al.  (2007). Cardiotoxicity associated with 
tyrosine kinase inhibitor sunitinib.  Lancet.  370:2011-2019. 
40. Khakoo, A.Y., C.M. Kassiotis , N. Tannir et al. (2008). Heart failure associated with 
sunitinib malate: a multitargeted receptor tyrosine kinase inhibitor. Cancer.  
112(11):2500-2508. 
41. Schmidinger, M., C.C. Zielinski, U.M. Vogl, et al. (2008).  Cardiac toxicity of sunitinib 
and sorafenib in patients with metastatic renal cell carcinoma. J Clin Oncol. 
26(32):5204-12. 
42. Telli, M.L., R.M. Witteles, G.A. Fisher, and S. Srinivas. (2008). Cardiotoxicity 
associated with the cancer therapeutic agent sunitinib malate. Ann Oncol. 
19(9):1613-8. 
43. Rini, B.I., I. Tamaskar, P. Shaheen, et al.  (2007). Hypothyroidism in patients with 
metastatic renal cell carcinoma treated with sunitinib.  J Natl Cancer Inst.  99:81-83. 
44. Desai, J., L. Yassa, E. Marqusee, et al.  (2006). Hypothyroidism after sunitinib 
treatment for patients with gastrointestinal stromal tumors.  Ann Inter Med.  145:660-
664. 
45. Demetri GD, van Oosterom AT, Garrett CR et al. Efficacy and safety of sunitinib in 
patients with advanced gastrointestinal stromal tumour after failure of imatinib: a 
randomized controlled trial. Lancet 2006; 368: 1329-38. 
46. Carvajal RD, Antonescu CR, Wolchok JD et al. Kit as a therapeutic target in 
metastatic melanoma. JAMA 2011; 305: 2327-34. 
47. Guo J, Si L, Kong Y et al. Phase II, open-label, single-arm trial of imatinib mesylate 
in patients with metastatic melanoma harboring c-kit mutation or amplification. J Clin 
Oncol 2011; 29:2904-9. 
48. Hodi FS, Corless CL, Giobbie-Hurder A, Fletcher JA et al. Imatinib for melanomas 
harboring mutationally activated or amplified KIT arising on mucosal, acral, and 
chronically sun-damaged skin. J Clin Oncol 2013; 31: 3182-3190. 
49. Minor DR, Kashani-Sabet M, Garrido M, O’Day SJ et al. Sunitinib therapy for 
melanoma patients with KIT mutations. Clin Cancer Res 2012; 18: 1457-63. 

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Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
42 
50. Heinrich MC, Maki RG, Corless CL et al. Primary and secondary kinase genotypes 
correlate with the biological and clinical activity of sunitinib in imatinib-resistant 
gastrointestinal stromal tumor. J Clin Oncol 2008; 26: 5352-9. 
51. Gajiwala KS, Wu JC, Christensen J et al. Kit kinase mutants show unique 
mechanisms of drug resistance to imatinib and sunitinib in gastrointestinal stromal 
tumor patients. Proc Natl Acad Sci USA 2009; 106: 1542-7.  
52. Piccaluga PP, Malagola M, Rondoni M et al. Imatinib mesylate in the treatment of 
newly diagnosed or refractory/resistant c-kit positive acute myeloid leukemia. Results 
of an Italian multicentric phase II study. Haematologica 2007; 92: 1721-2. 
53. Cairoli R, Beghini A, Morello E et al. Imatinib mesylate in the treatment of core 
binding factor leukemias with kit mutations. A report of three cases. Leuk Res 2005; 
29: 397-400. 
54. Orfao A, Garcia-Montero AC, Sanchez L, Escribano L. Recent advances in the 
understanding of mastocytosis: the role of KIT mutations. Brit J Haematol 2007; 138: 
12-30. 
55. Roussidis AE, Theocharis AD, Tzanakakis GN, Karamanos NK. The importance of c-
Kit and PDGF receptors as potential targets for molecular therapy in breast cancer. 
Curr Med Chem 2007; 14: 735-743. 
56. Macedo LT, Lima JP, dos Santos LV, Sasse AD. Prevention strategies for 
chemotherapy-induced hand-foot syndrome: a systematic review and meta-analysis 
of prospective randomised trials. Support Care Cancer. 2014 Jun;22(6):1585-93.  
PMID: 24463616. 
 

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Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
43 
Molecular Analysis for Therapy Choice (MATCH) 
MATCH Treatment Subprotocol V: Sunitinib 
Appendix I 
 
Patient Pill Calendar 
Storage: Store at Room Temperature 
Pill Calendar Directions 
1. Take your scheduled dose of each capsule. 
2. Take the capsules with or without food once daily for 28 days, and then take no 
study medicine for 14 days (rest days). Each cycle is 42 days long. 
3. If you forget, the missed capsules will not be taken later. 
4. Please bring the empty bottle or any leftover capsules and your pill calendar to your 
next clinic visit. 
5. Swallow capsules whole. Do not crush, chew or open capsules. 
 
Rev.12/16 
Rev.3/17 

ECOG-ACRIN 
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Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
44 
Patient Pill Calendar 
This is a calendar on which you are to record the time and number of capsules you take 
each day.  You should take your scheduled dose of each capsule. Note the times and 
the number of capsules that you take each day. If you develop any side effects, 
please record them and anything you would like to tell the doctor in the space provided.  
Bring any unused capsules and your completed pill calendar to your doctor’s visits. 
Sunitinib 
DAY 
Date 
Time 
capsules 
taken 
Number 
of 
capsules 
taken 
Use the space below to make notes about 
things you would like to tell the doctor (including 
unusual symptoms you experience, other 
medicine you have taken and anything else you 
think would be of interest.) 
Month 
Day 
Year 
1 
 
 
 
 
 
 
2 
 
 
 
 
 
 
3 
 
 
 
 
 
 
4 
 
 
 
 
 
 
5 
 
 
 
 
 
 
6 
 
 
 
 
 
 
7 
 
 
 
 
 
 
8 
 
 
 
 
 
 
9 
 
 
 
 
 
 
10 
 
 
 
 
 
 
11 
 
 
 
 
 
 
12 
 
 
 
 
 
 
13 
 
 
 
 
 
 
14 
 
 
 
 
 
 
15 
 
 
 
 
 
 
16 
 
 
 
 
 
 
17 
 
 
 
 
 
 
18 
 
 
 
 
 
 
19 
 
 
 
 
 
 
20 
 
 
 
 
 
 
21 
 
 
 
 
 
 
22 
 
 
 
 
 
 
23 
 
 
 
 
 
 
24 
 
 
 
 
 
 
25 
 
 
 
 
 
 
26 
 
 
 
 
 
 
27 
 
 
 
 
 
 
28 
 
 
 
 
 
 
Days 29-42 are rest days - Do not take any capsules 
Patient Signature: __________________________________ Date: _____________ 
Rev.2/16 

ECOG-ACRIN 
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Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
45 
Molecular Analysis for Therapy Choice (MATCH) 
MATCH Treatment Subprotocol V: Sunitinib 
Appendix II 
 
Actionable Mutations of Interest (aMOIs) 
List of Inclusion Variants: 
A function has been implemented in MATCHBOX to identify any in-frame insertions and 
deletions in exon 9, 11, 13, and 14 of the KIT gene at Level of Evidence code 2. This function 
may include any in-frame insertions, deletions or known activating missense mutations in exons 
9, 11, 13, and 14 of the KIT gene at Level of Evidence code 2. Please refer to Section 1.4.2 of 
the MATCH Master Protocol for more information. 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
KIT 
COSM1326 
Large Indel 
2 
p.S501_A502insAY 
KIT 
COSM27901 
Large Indel 
2 
p.P551_V560delinsL 
KIT 
COSM1198 
Large Indel 
2 
p.V555_V559del 
KIT 
COSM1230 
Large Indel 
2 
p.W557_V560delinsF 
KIT 
COSM1234 
Large Indel 
2 
p.K558_V560del 
KIT 
COSM1238 
Large Indel 
2 
p.K558_N564del 
KIT 
COSM1235 
Large Indel 
2 
p.K558_V559del 
KIT 
COSM1248 
Large Indel 
2 
p.V559_V560del 
KIT 
COSM1262 
Indel 
2 
p.E561del 
KIT 
COSM23560 
Large Indel 
2 
p.N564_Y578del 
KIT 
COSM1281 
Large Indel 
2 
p.V569_Q575del 
KIT 
COSM144983 
Large Indel 
2 
p.T500_S501insSA 
KIT 
COSM219786 
Large Indel 
2 
p.T500_S501insSA 
KIT 
COSM53306 
Large Indel 
2 
p.S501_A502insAF 
KIT 
COSM1164 
Large Indel 
2 
p.K550_V555delinsI 
KIT 
COSM1172 
Large Indel 
2 
p.P551_E554del 
KIT 
COSM1169 
Large Indel 
2 
p.Pro551_Val555del 
KIT 
COSM1170 
Large Indel 
2 
p.P551_Q556del 
KIT 
COSM1171 
Indel 
2 
p.P551del 
KIT 
COSM1174 
Large Indel 
2 
p.P551_V555delinsL 
KIT 
COSM1176 
Indel 
2 
p.P551_M552delinsL 
KIT 
COSM36304 
Large Indel 
2 
p.M552_D572del 
KIT 
COSM1177 
Large Indel 
2 
p.M552_W557del 
KIT 
COSM96881 
Large Indel 
2 
p.M552_Y553del 
KIT 
COSM1182 
Large Indel 
2 
p.M552_K558del 
KIT 
COSM1180 
Large Indel 
2 
p.M552_W557del 
KIT 
COSM18827 
Large Indel 
2 
p.M552_V555del 
KIT 
COSM1179 
Large Indel 
2 
p.M552_Y553del 
KIT 
COSM1181 
Large Indel 
2 
p.M552_E554del 
Rev. Add13 
Rev. Add19 
Rev.Add25 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
46 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
KIT 
COSM1327 
Large Indel 
2 
p.M552_Q556del 
KIT 
COSM96880 
Large Indel 
2 
p.M552_E561delinsK 
KIT 
COSM36311 
Large Indel 
2 
p.M552_E554delinsK 
KIT 
COSM96868 
Large Indel 
2 
p.M552_Q556delinsK 
KIT 
COSM96863 
Indel 
2 
p.M552_Y553delinsN 
KIT 
COSM133636 
Large Indel 
2 
p.M552_W557delinsR 
KIT 
COSM1185 
Large Indel 
2 
p.M552_V555delinsI 
KIT 
COSM1190 
Large Indel 
2 
p.M552_W557del 
KIT 
COSM1187 
Large Indel 
2 
p.M552_W557delinsK 
KIT 
COSM1189 
Large Indel 
2 
p.M552_Q556delinsK 
KIT 
COSM1191 
Large Indel 
2 
p.Y553_V559del 
KIT 
COSM22275 
Large Indel 
2 
p.Y553_T574delinsS 
KIT 
COSM96947 
Large Indel 
2 
p.E554_N564del 
KIT 
COSM36294 
Large Indel 
2 
p.E554_D572del 
KIT 
COSM36310 
Large Indel 
2 
p.E554_E562del 
KIT 
COSM36291 
Large Indel 
2 
p.E554_I571del 
KIT 
COSM1194 
Large Indel 
2 
p.E554_E561del 
KIT 
COSM1192 
Large Indel 
2 
p.E554_K558del 
KIT 
COSM1203 
Large Indel 
2 
p.V555_P573del 
KIT 
COSM37027 
Large Indel 
2 
p.E554_N564del 
KIT 
COSM1196 
Large Indel 
2 
p.V555_I563del 
KIT 
COSM1200 
Large Indel 
2 
p.V555_I571del 
KIT 
COSM1197 
Large Indel 
2 
p.V555_Y570del 
KIT 
COSM1202 
Large Indel 
2 
p.V555_V560del 
KIT 
COSM1199 
Large Indel 
2 
p.V555_K558del 
KIT 
COSM1201 
Large Indel 
2 
p.V555_Q556del 
KIT 
COSM96870 
Large Indel 
2 
p.V555_N566delinsD 
KIT 
COSM1209 
Large Indel 
2 
p.Q556_T574del 
KIT 
COSM36308 
Large Indel 
2 
p.Q556_P573del 
KIT 
COSM1205 
Large Indel 
2 
p.Q556_L576del 
KIT 
COSM36309 
Large Indel 
2 
p.Q556_W557del 
KIT 
COSM1206 
Large Indel 
2 
p.Q556_E561del 
KIT 
COSM1204 
Large Indel 
2 
p.Q556_V560del 
KIT 
COSM36315 
Large Indel 
2 
p.Q556_V559del 
KIT 
COSM23418 
Large Indel 
2 
p.Q556_K558del 
KIT 
COSM1212 
Large Indel 
2 
p.Q556_D572delinsH 
KIT 
COSM36312 
Large Indel 
2 
p.W557_E562del 
KIT 
COSM1330 
Large Indel 
2 
p.W557_E561del 
KIT 
COSM1210 
Large Indel 
2 
p.W557_K558del 
KIT 
COSM133642 
Indel 
2 
p.Q556_W557delinsR 
KIT 
COSM1365 
Large Indel 
2 
p.W557_I571del 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
47 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
KIT 
COSM1221 
SNV 
2 
p.W557G 
KIT 
COSM1220 
Indel 
2 
p.W557del 
KIT 
COSM1213 
Large Indel 
2 
p.Q556_V560delinsH 
KIT 
COSM133641 
Large Indel 
2 
p.Q556_V559delinsH 
KIT 
COSM1214 
Large Indel 
2 
p.Q556_V559delinsHT 
KIT 
COSM133639 
Large Indel 
2 
p.W557_Q575del 
KIT 
COSM1223 
Large Indel 
2 
p.W557_V560del 
KIT 
COSM1218 
Large Indel 
2 
p.W557_V559del 
KIT 
COSM24748 
Indel 
2 
p.W557_K558delinsE 
KIT 
COSM1229 
Large Indel 
2 
p.W557_P573delinsS 
KIT 
COSM1226 
Large Indel 
2 
p.W557_V559delinsF 
KIT 
COSM1239 
Large Indel 
2 
p.K558_E562del 
KIT 
COSM1232 
Large Indel 
2 
p.W557_V560delinsC 
KIT 
COSM1233 
Large Indel 
2 
p.W557_V559delinsC 
KIT 
COSM36303 
Large Indel 
2 
p.K558_Q575del 
KIT 
COSM1236 
Large Indel 
2 
p.K558_G565del 
KIT 
COSM1237 
Large Indel 
2 
p.K558_D572del 
KIT 
COSM28991 
Large Indel 
2 
p.K558_Y570delinsN 
KIT 
COSM1250 
Large Indel 
2 
p.V559_E561del 
KIT 
COSM1240 
Large Indel 
2 
p.K558_G565delinsR 
KIT 
COSM1241 
Large Indel 
2 
p.K558_V560delinsI 
KIT 
COSM27069 
Large Indel 
2 
p.K558_V560delinsN 
KIT 
COSM21976 
Indel 
2 
p.K558delinsNP 
KIT 
COSM1244 
Indel 
2 
p.K558_V559delinsN 
KIT 
COSM1245 
Indel 
2 
p.K558delinsNP 
KIT 
COSM36300 
Large Indel 
2 
p.V559_L576del 
KIT 
COSM1249 
Large Indel 
2 
p.V559_G565del 
KIT 
COSM36301 
Large Indel 
2 
p.V559_I571del 
KIT 
COSM1247 
Indel 
2 
p.V559del 
KIT 
COSM1252 
SNV 
2 
p.V559D 
KIT 
COSM36293 
Large Indel 
2 
p.V560_L576del 
KIT 
COSM1257 
SNV 
2 
p.V560D 
KIT 
COSM1260 
SNV 
2 
p.V560G 
KIT 
COSM30545 
Large Indel 
2 
p.V559_P573delinsA 
KIT 
COSM18897 
Large Indel 
2 
p.V559_E562del 
KIT 
COSM133640 
Large Indel 
2 
p.V560_I571del 
KIT 
COSM29442 
Large Indel 
2 
p.I563_L576del 
KIT 
COSM1268 
Large Indel 
2 
p.I563_D572del 
KIT 
COSM24839 
Large Indel 
2 
p.N564_T574del 
KIT 
COSM1270 
Large Indel 
2 
p.N564_L576del 
KIT 
COSM1269 
Large Indel 
2 
p.N564_P577del 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
48 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
KIT 
COSM36299 
Large Indel 
2 
p.N564_P573delinsT 
KIT 
COSM133635 
Large Indel 
2 
p.V569_L576del 
KIT 
COSM1282 
Large Indel 
2 
p.V569_D572del 
KIT 
COSM1285 
Large Indel 
2 
p.Y570_L576del 
KIT 
COSM29016 
Large Indel 
2 
p.I571_N587del 
KIT 
COSM29857 
Large Indel 
2 
p.Y570_I571insIDPTQLPYDHKWEFPS
D 
KIT 
COSM41198 
Large Indel 
2 
p.Y570_I571insIDPTQLPYDH 
KIT 
COSM133754 
Large Indel 
2 
p.I571_L576del 
KIT 
COSM23417 
Large Indel 
2 
p.Y570_I571insIDPTQLPYD 
KIT 
COSM308544 
Large Indel 
2 
p.I571_D572insDPTQLPYD 
KIT 
COSM18751 
Large Indel 
2 
p.I571_D572insDPTQLPYDHKWEF 
KIT 
COSM30595 
Large Indel 
2 
p.I571_D572insDPTQLPYDHKWEFP 
KIT 
COSM34126 
Large Indel 
2 
p.D572_P573insPTQLPYDH 
KIT 
COSM36322 
Large Indel 
2 
p.D572_P573insPTQLPYDHKWEFP 
KIT 
COSM18668 
Large Indel 
2 
p.D572_P573insPTQLPYD 
KIT 
COSM33906 
Large Indel 
2 
p.D572_P573insPTQLPYDHKWEF 
KIT 
COSM1289 
Indel 
2 
p.L576del 
KIT 
COSM1300 
Large Indel 
2 
p.Q575_L576insLPYDHKWEFP 
KIT 
COSM1298 
Large Indel 
2 
p.Q575_L576insLPYDHKWEF 
KIT 
COSM41632 
Large Indel 
2 
p.L576_P577insPYDHKWEF 
KIT 
COSM1290 
SNV 
2 
p.L576P 
KIT 
COSM98379 
Large Indel 
2 
p.P577_D579del 
KIT 
COSM1296 
Large Indel 
2 
p.L576_P577insPYDH 
KIT 
COSM1291 
Large Indel 
2 
p.P577_Y578del 
KIT 
COSM1684822 
Indel 
2 
p.P577de 
KIT 
COSM18666 
Large Indel 
2 
p.L576_P577insPYDH 
KIT 
COSM96866 
Large Indel 
2 
p.D579_H580insSYD 
KIT 
COSM28995 
Large Indel 
2 
p.P577_Y578insYDH 
KIT 
COSM1294 
Indel 
2 
p.D579del 
KIT 
COSM1295 
Indel 
2 
p.H580del 
KIT 
COSM36323 
Large Indel 
2 
p.F584_P585insIDPTQLPYDHKWEFR 
KIT 
COSM1304 
SNV 
2 
p.K642E 
KIT 
COSM12706 
SNV 
2 
p.V654A 
KIT 
COSM1253 
SNV 
2 
p.V559G 
KIT 
COSM12708 
SNV 
2 
p.T670I 
KIT 
COSM4383740 
SNV 
3 
p.S476N 
KIT 
COSM219784 
SNV 
3 
p.S476I 
KIT 
COSM327599 
SNV 
3 
p.E490K 
KIT 
COSM6957947 
SNV 
3 
p.D496N 
KIT 
COSM133685 
SNV 
3 
p.T500I 
KIT 
COSM96885 
SNV 
3 
p.K509I 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
49 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
KIT 
COSM133699 
SNV 
3 
p.G510D 
KIT 
COSM5686734 
SNV 
3 
p.P551A 
KIT 
COSM1183 
SNV 
3 
p.M552L 
KIT 
COSM734168 
SNV 
3 
p.M552L 
KIT 
COSM133763 
SNV 
3 
p.Y553N 
KIT 
COSM1216 
SNV 
3 
p.W557R 
KIT 
COSM1219 
SNV 
3 
p.W557R 
KIT 
COSM133700 
SNV 
3 
p.W557C 
KIT 
COSM19108 
SNV 
3 
p.W557C 
KIT 
COSM30551 
SNV 
3 
p.K558E 
KIT 
COSM1246 
SNV 
3 
p.K558N 
KIT 
COSM1255 
SNV 
3 
p.V559A 
KIT 
COSM1253 
SNV 
3 
p.V559G 
KIT 
COSM36302 
SNV 
3 
p.V560A 
KIT 
COSM1264 
SNV 
3 
p.E561K 
KIT 
COSM133701 
SNV 
3 
p.R586K 
KIT 
COSM5702513 
SNV 
3 
p.S628N 
KIT 
COSM1600403 
SNV 
3 
p.R634W 
KIT 
COSM96871 
SNV 
3 
p.K642Q 
KIT 
COSM133675 
SNV 
3 
p.G663E 
KIT 
COSM36053 
SNV 
3 
p.H697Y 
KIT 
MVAR183 
SNV 
3 
p.H802T 
KIT 
COSM18681 
SNV 
3 
p.Y823D 
KIT 
COSM24637 
SNV 
3 
p.F469L 
KIT 
COSM24639 
SNV 
3 
p.N486D 
KIT 
COSM24638 
SNV 
3 
p.V489A 
KIT 
COSM29015 
SNV 
3 
p.K558R 
KIT 
COSM1246 
SNV 
3 
p.K558N 
PDGFRA 
MVAR189 
Indel 
3 
p.W559_R560del 
PDGFRA 
COSM739 
SNV 
3 
p.V561D 
PDGFRA 
COSM742 
Indel 
3 
p.S566_E571>R 
PDGFRA 
COSM12418 
Indel 
3 
p.S566_E571>R 
PDGFRA 
COSM30546 
Indel 
3 
p.S566_E571>R 
PDGFRA 
COSM22414 
SNV 
3 
p.N659K 
PDGFRA 
COSM22415 
SNV 
3 
p.N659K 
PDGFRA 
COSM743 
SNV 
3 
P.T674I 
PDGFRA 
COSM12397 
SNV 
3 
p.D842Y 
PDGFRA 
COSM737 
Indel 
3 
p.I843_D846delIMHD 
PDGFRA 
COSM12396 
SNV 
3 
p.D842Y 
PDGFRA 
COSM96892 
Indel 
3 
p.I843_D846delIMHD 
PDGFRA 
COSM12400 
Indel 
3 
p.I843_D846delIMHD 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
50 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
PDGFRA 
COSM12407 
Indel 
3 
p.I843_S847>T 
PDGFRA 
COSM4969655 
Indel 
3 
p.I843delI 
PDGFRA 
COSM738 
Indel 
3 
p.H845_N848>P 
PDGFRA 
COSM12399 
SNV 
3 
p.D846Y 
PDGFRA 
COSM94952 
SNV 
3 
p.Y849C 
PDGFRB 
VCV00037555
7 
InDel 
3 
p.I538_L539insR 
PDGFRB 
VCV00005584
8 
SNV 
3 
p.R561C 
PDGFRB 
VCV00037568
2 
SNV 
3 
p.W566R 
PDGFRB 
VCV00037555
5 
Indel 
3 
p.W566_V568delinsL 
PDGFRB 
COSM6916840 
SNV 
3 
p.N666K 
PDGFRB 
COSM6927334 
SNV 
3 
p.D850V 
PDGFRA 
BCR-
PDGFRA.B12i
ns12P12 
Fusion 
3 
BCR-PDGFRA.B12ins12P12 
PDGFRA 
BCR-
PDGFRA.B1P1
3 
Fusion 
3 
BCR-PDGFRA.B1P13 
PDGFRA 
BCR-
PDGFRA.B7in
s24P12 
Fusion 
3 
BCR-PDGFRA.B7ins24P12 
PDGFRA 
CDK5RAP2-
PDGFRA.C13i
ns40P12 
Fusion 
3 
CDK5RAP2-PDGFRA.C13ins40P12 
PDGFRA 
DIP2C-
PDGFRA.D1P
10 
Fusion 
3 
DIP2C-PDGFRA.D1P10 
PDGFRA 
DIP2C-
PDGFRA.D1P
11 
Fusion 
3 
DIP2C-PDGFRA.D1P11 
PDGFRA 
ETV6-
PDGFRA.E6P1
2 
Fusion 
3 
ETV6-PDGFRA.E6P12 
PDGFRA 
FIP1L1-
PDGFRA.F10P
12del47 
Fusion 
3 
FIP1L1-PDGFRA.F10P12del47 
PDGFRA 
FIP1L1-
PDGFRA.F10i
nt10P12del106 
Fusion 
3 
FIP1L1-PDGFRA.F10int10P12del106 
PDGFRA 
FIP1L1-
PDGFRA.F10i
nt10P12del22 
Fusion 
3 
FIP1L1-PDGFRA.F10int10P12del22 
PDGFRA 
FIP1L1-
PDGFRA.F10i
nt10P12del67 
Fusion 
3 
FIP1L1-PDGFRA.F10int10P12del67 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
51 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
PDGFRA 
FIP1L1-
PDGFRA.F11P
12del24 
Fusion 
3 
FIP1L1-PDGFRA.F11P12del24 
PDGFRA 
FIP1L1-
PDGFRA.F11P
12del26 
Fusion 
3 
FIP1L1-PDGFRA.F11P12del26 
PDGFRA 
FIP1L1-
PDGFRA.F11P
12del45 
Fusion 
3 
FIP1L1-PDGFRA.F11P12del45 
PDGFRA 
FIP1L1-
PDGFRA.F11P
12del77 
Fusion 
3 
FIP1L1-PDGFRA.F11P12del77 
PDGFRA 
FIP1L1-
PDGFRA.F11P
12del77.1 
Fusion 
3 
FIP1L1-PDGFRA.F11P12del77.1 
PDGFRA 
FIP1L1-
PDGFRA.F12P
12del107 
Fusion 
3 
FIP1L1-PDGFRA.F12P12del107 
PDGFRA 
FIP1L1-
PDGFRA.F12P
12del84 
Fusion 
3 
FIP1L1-PDGFRA.F12P12del84 
PDGFRA 
FIP1L1-
PDGFRA.F13P
12del71 
Fusion 
3 
FIP1L1-PDGFRA.F13P12del71 
PDGFRA 
FIP1L1-
PDGFRA.F13P
12del75 
Fusion 
3 
FIP1L1-PDGFRA.F13P12del75 
PDGFRA 
FIP1L1-
PDGFRA.F13i
ns11P12del99 
Fusion 
3 
FIP1L1-PDGFRA.F13ins11P12del99 
PDGFRA 
FIP1L1-
PDGFRA.F13i
nsP12del91 
Fusion 
3 
FIP1L1-PDGFRA.F13insP12del91 
PDGFRA 
FIP1L1-
PDGFRA.F16i
ns16P12del71 
Fusion 
3 
FIP1L1-PDGFRA.F16ins16P12del71 
PDGFRA 
FIP1L1-
PDGFRA.F9P1
2del38 
Fusion 
3 
FIP1L1-PDGFRA.F9P12del38 
PDGFRA 
FOXP1-
PDGFRA.F16P
12 
Fusion 
3 
FOXP1-PDGFRA.F16P12 
PDGFRA 
KDR-
PDGFRA.K13i
ns35P10 
Fusion 
3 
KDR-PDGFRA.K13ins35P10 
PDGFRA 
KIF5B-
PDGFRA.K23P
12 
Fusion 
3 
KIF5B-PDGFRA.K23P12 
PDGFRA 
SCAF11-
PDGFRA.S1P2 
Fusion 
3 
SCAF11-PDGFRA.S1P2 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
52 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
PDGFRA 
STRN-
PDGFRA.S6P1
2 
Fusion 
3 
STRN-PDGFRA.S6P12 
PDGFRA 
STRN-
PDGFRA.S6P1
2.1 
Fusion 
3 
STRN-PDGFRA.S6P12.1 
PDGFRA 
TNKS2-
PDGFRA.T25P
12 
Fusion 
3 
TNKS2-PDGFRA.T25P12 
PDGRB 
ATF7IP-
PDGFRB.A13P
11 
Fusion 
3 
ATF7IP-PDGFRB.A13P11 
PDGRB 
BIN2-
PDGFRB.B9P1
2 
Fusion 
3 
BIN2-PDGFRB.B9P12 
PDGRB 
CAPRIN1-
PDGFRB.C7P
11 
Fusion 
3 
CAPRIN1-PDGFRB.C7P11 
PDGRB 
CCDC6-
PDGFRB.C7P
11 
Fusion 
3 
CCDC6-PDGFRB.C7P11 
PDGRB 
CCDC88C-
PDGFRB.C10
P12 
Fusion 
3 
CCDC88C-PDGFRB.C10P12 
PDGRB 
CCDC88C-
PDGFRB.C12
P11 
Fusion 
3 
CCDC88C-PDGFRB.C12P11 
PDGRB 
CCDC88C-
PDGFRB.C25
P11 
Fusion 
3 
CCDC88C-PDGFRB.C25P11 
PDGRB 
CEP85L-
PDGFRB.C11
P12 
Fusion 
3 
CEP85L-PDGFRB.C11P12 
PDGRB 
CPSF6-
PDGFRB.C5P
11 
Fusion 
3 
CPSF6-PDGFRB.C5P11 
PDGRB 
DTD1-
PDGFRB.D4P
12 
Fusion 
3 
DTD1-PDGFRB.D4P12 
PDGRB 
EBF1-
PDGFRB.E11P
11 
Fusion 
3 
EBF1-PDGFRB.E11P11 
PDGRB 
EBF1-
PDGFRB.E14P
11 
Fusion 
3 
EBF1-PDGFRB.E14P11 
PDGRB 
EBF1-
PDGFRB.E15P
11 
Fusion 
3 
EBF1-PDGFRB.E15P11 
PDGRB 
ERC1-
PDGFRB.E15P
10 
Fusion 
3 
ERC1-PDGFRB.E15P10 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
53 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
PDGRB 
ERC1-
PDGFRB.E15P
11 
Fusion 
3 
ERC1-PDGFRB.E15P11 
PDGRB 
ETV6-
PDGFRB.E4P1
1 
Fusion 
3 
ETV6-PDGFRB.E4P11 
PDGRB 
ETV6-
PDGFRB.E4P9 
Fusion 
3 
ETV6-PDGFRB.E4P9 
PDGRB 
ETV6-
PDGFRB.E7P1
0 
Fusion 
3 
ETV6-PDGFRB.E7P10 
PDGRB 
ETV6-
PDGFRB.E7in
s34P12 
Fusion 
3 
ETV6-PDGFRB.E7ins34P12 
PDGRB 
GIT2-
PDGFRB.G12
P11 
Fusion 
3 
GIT2-PDGFRB.G12P11 
PDGRB 
GOLGA4-
PDGFRB.G10
P11 
Fusion 
3 
GOLGA4-PDGFRB.G10P11 
PDGRB 
GOLGB1-
PDGFRB.G10
P12 
Fusion 
3 
GOLGB1-PDGFRB.G10P12 
PDGRB 
HIP1-
PDGFRB.H30
P11 
Fusion 
3 
HIP1-PDGFRB.H30P11 
PDGRB 
KANK1-
PDGFRB.K2P9 
Fusion 
3 
KANK1-PDGFRB.K2P9 
PDGRB 
MPRIP-
PDGFRB.M20
P12 
Fusion 
3 
MPRIP-PDGFRB.M20P12 
PDGRB 
MYO18A-
PDGFRB.M41
P10 
Fusion 
3 
MYO18A-PDGFRB.M41P10 
PDGRB 
NDE1-
PDGFRB.N6P
11 
Fusion 
3 
NDE1-PDGFRB.N6P11 
PDGRB 
NIN-
PDGFRB.N30
P12 
Fusion 
3 
NIN-PDGFRB.N30P12 
PDGRB 
PDE4DIP-
PDGFRB.P16P
11 
Fusion 
3 
PDE4DIP-PDGFRB.P16P11 
PDGRB 
PRKG2-
PDGFRB.P3P1
2 
Fusion 
3 
PRKG2-PDGFRB.P3P12 
PDGRB 
PRKG2-
PDGFRB.P6P1
2 
Fusion 
3 
PRKG2-PDGFRB.P6P12 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
54 
Gene Name 
Variant ID 
Variant 
Type 
Level of Evidence 
Code 
aMOI 
PDGRB 
RABEP1-
PDGFRB.R14
P11 
Fusion 
3 
RABEP1-PDGFRB.R14P11 
PDGRB 
SART3-
PDGFRB.S15P
11 
Fusion 
3 
SART3-PDGFRB.S15P11 
PDGRB 
SPECC1-
PDGFRB.S3P1
1 
Fusion 
3 
SPECC1-PDGFRB.S3P11 
PDGRB 
TNIP1-
PDGFRB.T14P
11 
Fusion 
3 
TNIP1-PDGFRB.T14P11 
PDGRB 
TP53BP1-
PDGFRB.T23P
11 
Fusion 
3 
TP53BP1-PDGFRB.T23P11 
PDGRB 
TPM3-
PDGFRB.T7P1
1 
Fusion 
3 
TPM3-PDGFRB.T7P11 
PDGRB 
TRIP11-
PDGFRB.T16P
11 
Fusion 
3 
TRIP11-PDGFRB.T16P11 
PDGRB 
WDR48-
PDGFRB.W9P
12 
Fusion 
3 
WDR48-PDGFRB.W9P12 
PDGRB 
ZEB2-
PDGFRB.Z9P9 
Fusion 
3 
ZEB2-PDGFRB.Z9P9 
List of Exclusion Variants: 
Gene Name 
Variant ID 
Variant Type 
Level of Evidence 
Code 
aMOI 
KIT 
COSM1311 
SNV 
2 
p.D816H 
KIT 
COSM1310 
SNV 
2 
p.D816Y 
KIT 
COSM24675 
SNV 
2 
p.D816A 
KIT 
COSM12711 
SNV 
3 
p.D816G 
KIT 
COSM1314 
SNV 
2 
p.D816V 
KIT 
COSM19285 
SNV 
3 
p.D816E 
KIT 
COSM12710 
SNV 
2 
p.D820Y 
KIT 
COSM133670 
SNV 
2 
p.D820A 
KIT 
COSM1316 
SNV 
2 
p.D820G 
KIT 
COSM12709 
SNV 
2 
p.D820E 
KIT 
COSM19280 
SNV 
2 
p.D820E 
KIT 
COSM1318 
SNV 
2 
p.N822H 
KIT 
COSM1321 
SNV 
2 
p.N822K 
KIT 
COSM1322 
SNV 
2 
p.N822K 
KIT 
COSM18681 
SNV 
2 
p.Y823D 
KIT 
COSM13172 
SNV 
2 
p.A829P 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
55 
 

ECOG-ACRIN 
EAY131-V 
Cancer Research Group 
Version Date: November 10, 2022 
 
NCI Update Date: August 12, 2015 
56 
Molecular Analysis for Therapy Choice (MATCH) 
MATCH Treatment Subprotocol V: Sunitinib 
Appendix III 
 
Medications That May Cause QTc Prolongation 
Drugs that are generally 
accepted to have a risk of 
causing Torsades de 
Pointes 
Drugs that in some reports have 
been associated with Torsades 
de Pointes and/or QTc 
prolongation but at this time lack 
substantial evidence for causing 
Torsades de Pointes 
Drugs that, in some reports, have been weakly 
associated with Torsades de Pointes and/or QTc 
prolongation but that are unlikely to be a risk for 
Torsades de Pointes when used in usual 
recommended dosages and in subjects without 
other risk factors (e.g., concomitant QTc 
prolonging drugs, bradycardia, electrolyte 
disturbances, congenital long QTc syndrome, 
concomitant drugs that inhibit metabolism) 
Generic/Brand Name 
Generic/Brand Name 
Generic/Brand Name 
Amiodarone /Cordarone® 
Alfuzosin /Uroxatral® 
Amitriptyline /Elavil® 
Amiodarone /Pacerone® 
Amantadine /Symmetrel® 
Ciprofloxacin /Cipro® 
Arsenic trioxide 
/Trisenox® 
Atazanavir /Reyataz® 
Citalopram /Celexa® 
Astemizole /Hismanal® 
Azithromycin /Zithromax® 
Clomipramine /Anafranil® 
Bepridil /Vascor® 
Chloral hydrate /Noctec® 
Desipramine /Pertofrane® 
Chloroquine /Aralen® 
Clozapine /Clozaril® 
Diphenhydramine /Benadryl® 
Chlorpromazine 
/Thorazine® 
Dolasetron /Anzemet® 
Diphenhydramine /Nytol® 
Cisapride /Propulsid® 
Dronedarone /Multaq® 
Doxepin /Sinequan® 
Clarithromycin /Biaxin® 
Felbamate /Felbatrol® 
Fluconazole /Diflucan® 
Disopyramide /Norpace® 
Flecainide /Tambocor® 
Fluoxetine /Sarafem® 
Dofetilide /Tikosyn® 
Foscarnet /Foscavir® 
Fluoxetine /Prozac® 
Domperidone /Motilium® 
Fosphenytoin /Cerebyx® 
Galantamine /Reminyl® 
Droperidol /Inapsine® 
Gatifloxacin /Tequin® 
Imipramine /Norfranil® 
Erythromycin /Erythrocin® 
Gemifloxacin /Factive® 
Itraconazole /Sporanox® 
Erythromycin /E.E.S.® 
Granisetron /Kytril® 
Ketoconazole /Nizoral® 
Halofantrine /Halfan® 
Indapamide /Lozol® 
Mexiletine /Mexitil® 
Haloperidol /Haldol® 
Isradipine /Dynacirc® 
Nortriptyline /Pamelor® 
Ibutilide /Corvert® 
Lapatinib /Tykerb® 
Paroxetine /Paxil® 
Levomethadyl /Orlaam® 
Lapatinib /Tyverb® 
Protriptyline /Vivactil® 
Mesoridazine /Serentil® 
Levofloxacin /Levaquin® 
Sertraline /Zoloft® 
Methadone /Dolophine® 
Lithium /Lithobid® 
Solifenacin /VESIcare® 
Methadone /Methadose® 
Lithium /Eskalith® 
Trimethoprim-Sulfa /Sulfa® 
Pentamidine /Pentam® 
Moexipril/HCTZ /Uniretic® 
Trimethoprim-Sulfa /Bactrim® 
Pentamidine /NebuPent® 
Moxifloxacin /Avelox® 
Trimipramine /Surmontil® 
Pimozide /Orap® 
Nicardipine /Cardene® 
  
Probucol /Lorelco® 
Nilotinib /Tasigna® 
  
Procainamide /Pronestyl® 
Octreotide /Sandostatin® 
  
Procainamide /Procan® 
Ofloxacin /Floxin® 
  

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Drugs that are generally 
accepted to have a risk of 
causing Torsades de 
Pointes 
Drugs that in some reports have 
been associated with Torsades 
de Pointes and/or QTc 
prolongation but at this time lack 
substantial evidence for causing 
Torsades de Pointes 
Drugs that, in some reports, have been weakly 
associated with Torsades de Pointes and/or QTc 
prolongation but that are unlikely to be a risk for 
Torsades de Pointes when used in usual 
recommended dosages and in subjects without 
other risk factors (e.g., concomitant QTc 
prolonging drugs, bradycardia, electrolyte 
disturbances, congenital long QTc syndrome, 
concomitant drugs that inhibit metabolism) 
Generic/Brand Name 
Generic/Brand Name 
Generic/Brand Name 
Quinidine /Cardioquin® 
Ondansetron /Zofran® 
  
Quinidine /Quinaglute® 
Oxytocin /Pitocin® 
  
Sotalol /Betapace® 
Paliperidone /Invega® 
  
Sparfloxacin /Zagam® 
Perflutren lipid microspheres 
/Definity® 
  
Terfenadine /Seldane® 
Quetiapine /Seroquel® 
  
Thioridazine /Mellaril® 
Ranolazine /Ranexa® 
  
  
Risperidone /Risperdal® 
  
  
Roxithromycin* /Rulide® 
  
  
Sertindole /Serlect® 
  
  
Sertindole /Serdolect® 
  
  
Sunitinib /Sutent® 
  
  
Tacrolimus /Prograf® 
  
  
Tamoxifen /Nolvadex® 
  
  
Telithromycin /Ketek® 
  
  
Tizanidine /Zanaflex® 
  
  
Vardenafil /Levitra® 
  
  
Venlafaxine /Effexor® 
  
  
Voriconazole /VFend® 
  
  
Ziprasidone /Geodon® 
  
 

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Molecular Analysis for Therapy Choice (MATCH) 
MATCH Treatment Subprotocol V: Sunitinib 
Appendix IV 
 
NCI/DCTD Collaborative Agreements Language 
Protocols that involve agent(s) covered by a collaborative agreement with a biotech/pharma 
company(ies) must incorporate the NCI/ DCTD Collaborative Agreement Language shown 
below. 
The agent(s) supplied by CTEP, DCTD, NCI used in this protocol is/are provided to the NCI 
under a Collaborative Agreement (CRADA, CTA, CSA) between the Pharmaceutical 
Company(ies) (hereinafter referred to as “Collaborator(s)”) and the NCI Division of Cancer 
Treatment and Diagnosis.  Therefore, the following obligations/guidelines, in addition to the 
provisions in the “Intellectual Property Option to Collaborator” 
(http://ctep.cancer.gov/industryCollaborations2/intellectual_property.htm) contained within the 
terms of award, apply to the use of the Agent(s) in this study: 
1. Agent(s) may not be used for any purpose outside the scope of this protocol, nor can 
Agent(s) be transferred or licensed to any party not participating in the clinical study.  
Collaborator(s) data for Agent(s) are confidential and proprietary to Collaborator(s) and shall 
be maintained as such by the investigators. The protocol documents for studies utilizing 
Agents contain confidential information and should not be shared or distributed without the 
permission of the NCI.  If a copy of this protocol is requested by a patient or patient’s family 
member participating on the study, the individual should sign a confidentiality agreement. A 
suitable model agreement can be downloaded from: http://ctep.cancer.gov. 
2. For a clinical protocol where there is an investigational Agent used in combination with 
(an)other Agent(s), each the subject of different Collaborative Agreements, the access to 
and use of data by each Collaborator shall be as follows (data pertaining to such 
combination use shall hereinafter be referred to as "Multi-Party Data”): 
a. NCI will provide all Collaborators with prior written notice regarding the existence and 
nature of any agreements governing their collaboration with NCI, the design of the 
proposed combination protocol, and the existence of any obligations that would tend to 
restrict NCI's participation in the proposed combination protocol. 
b. Each Collaborator shall agree to permit use of the Multi-Party Data from the clinical trial 
by any other Collaborator solely to the extent necessary to allow said other Collaborator 
to develop, obtain regulatory approval or commercialize its own Agent. 
c. Any Collaborator having the right to use the Multi-Party Data from these trials must 
agree in writing prior to the commencement of the trials that it will use the Multi-Party 
Data solely for development, regulatory approval, and commercialization of its own 
Agent. 
3. Clinical Trial Data and Results and Raw Data developed under a Collaborative Agreement 
will be made available to Collaborator(s), the NCI, and the FDA, as appropriate and unless 
additional disclosure is required by law or court order as described in the IP Option to 
Collaborator (http://ctep.cancer.gov/industryCollaborations2/intellectual_property.htm). 
Additionally, all Clinical Data and Results and Raw Data will be collected, used and 
disclosed consistent with all applicable federal statutes and regulations for the protection of 

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human subjects, including, if applicable, the Standards for Privacy of Individually Identifiable 
Health Information set forth in 45 C.F.R. Part 164. 
4. When a Collaborator wishes to initiate a data request, the request should first be sent to the 
NCI, who will then notify the appropriate investigators (Group Chair for Cooperative Group 
studies, or PI for other studies) of Collaborator's wish to contact them. 
5. Any data provided to Collaborator(s) for Phase 3 studies must be in accordance with the 
guidelines and policies of the responsible Data Monitoring Committee (DMC), if there is a 
DMC for this clinical trial. 
6. Any manuscripts reporting the results of this clinical trial must be provided to CTEP by the 
Group office for Cooperative Group studies or by the principal investigator for non-
Cooperative Group studies for immediate delivery to Collaborator(s) for advisory review and 
comment prior to submission for publication. Collaborator(s) will have 30 days from the date 
of receipt for review.  Collaborator shall have the right to request that publication be delayed 
for up to an additional 30 days in order to ensure that Collaborator’s confidential and 
proprietary data, in addition to Collaborator(s)’s intellectual property rights, are protected.  
Copies of abstracts must be provided to CTEP for forwarding to Collaborator(s) for courtesy 
review as soon as possible and preferably at least three (3) days prior to submission, but in 
any case, prior to presentation at the meeting or publication in the proceedings. Press 
releases and other media presentations must also be forwarded to CTEP prior to release. 
Copies of any manuscript, abstract and/or press release/ media presentation should be sent 
to: 
Email: ncicteppubs@mail.nih.gov  
The Regulatory Affairs Branch will then distribute them to Collaborator(s).  No publication, 
manuscript or other form of public disclosure shall contain any of Collaborator’s confidential/ 
proprietary information. 

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Molecular Analysis for Therapy Choice (MATCH) 
MATCH Treatment Subprotocol V: Sunitinib 
Appendix V 
 
Patient Clinical Trial Wallet Card 
 
 
CLINICAL TRIAL WALLET CARD 
Show this card to all of your 
healthcare providers and keep 
it with you in case you go to 
the emergency room. 
Patient Name:        
Diagnosis:        
Study Doctor:       
Study Doctor Phone #:       
NCI Trial #:        
Study Drug(S):        
 
 
 
 
For more information: 1-800-4-CANCER 
cancer.gov | clinicaltrials.gov 
 
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