# EDGAR Filing Document

**Accession Number:** 0001815442
**File Stem:** 0001193125-25-132838
**Filing Date:** 2025-6
**Character Count:** 36735
**Document Hash:** 519c589cf41b3360895d03c03eba0add
**Contains OCR:** False
**Source Format:** 

## Filing Content

## Filing Summary
**0001193125-25-132838.hdr.sgml**: 20250602

**ACCESSION NUMBER**: 0001193125-25-132838

**CONFORMED SUBMISSION TYPE**: 8-K

**PUBLIC DOCUMENT COUNT**: 51

**CONFORMED PERIOD OF REPORT**: 20250602

**ITEM INFORMATION**: Regulation FD Disclosure

**ITEM INFORMATION**: Financial Statements and Exhibits

**FILED AS OF DATE**: 20250602

**DATE AS OF CHANGE**: 20250602

**FILER**: 

**COMPANY DATA:**
- **COMPANY CONFORMED NAME:** Kymera Therapeutics, Inc.
- **CENTRAL INDEX KEY:** 0001815442
- **STANDARD INDUSTRIAL CLASSIFICATION:** BIOLOGICAL PRODUCTS (NO DIAGNOSTIC SUBSTANCES) [2836]
- **ORGANIZATION NAME:** 03 Life Sciences
- **EIN:** 812992166
- **STATE OF INCORPORATION:** DE
- **FISCAL YEAR END:** 1231

**FILING VALUES:**
- **FORM TYPE:** 8-K
- **SEC ACT:** 1934 Act
- **SEC FILE NUMBER:** 001-39460
- **FILM NUMBER:** 251013218

**BUSINESS ADDRESS:**
- **STREET 1:** 500 NORTH BEACON STREET, 4TH FLOOR
- **CITY:** WATERTOWN
- **STATE:** MA
- **ZIP:** 02472
- **BUSINESS PHONE:** 857-285-5314

**MAIL ADDRESS:**
- **STREET 1:** 500 NORTH BEACON STREET, 4TH FLOOR
- **CITY:** WATERTOWN
- **STATE:** MA
- **ZIP:** 02472

?xml version='1.0' encoding='ASCII'? 8-K

### UNITED STATES

### SECURITIES AND EXCHANGE COMMISSION

#### Washington, D.C. 20549

### FORM 8-K

#### CURRENT REPORT

#### Pursuant to Section 13 or 15(d)

#### of the Securities Exchange Act of 1934

#### Date of Report (Date of earliest event reported): June 2, 2025

## KYMERA THERAPEUTICS, INC.

#### (Exact name of registrant as specified in its charter)

---

| | | |
|:---|:---|:---|
| **Delaware** | **001-39460** | **81-2992166** |
| **(State or other jurisdiction<br>of incorporation)** | **(Commission**<br> **File Number)** | **(I.R.S. Employer<br>Identification No.)** |

---

#### Kymera Therapeutics, Inc.

---

| |
|:---|
| **500 North Beacon Street, 4th Floor** |
| **Watertown, Massachusetts 02472** |
| **(Address of principal executive offices, including zip code)** |

---

(857) 285-5300

#### (Registrant's telephone number, including area code)

#### Not Applicable

#### (Former Name or Former Address, if Changed Since Last Report)
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

☐ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

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| | | |
|:---|:---|:---|
| **Title of each class** | **Trade**<br> **Symbol(s)** | **Name of each exchange**<br> **on which registered** |
| Common Stock, $0.0001 par value per share | KYMR | The Nasdaq Global Market |

---

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).

Emerging growth company ☐

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

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| | |
|:---|:---|
| **Item 7.01** | **Regulation FD Disclosure.**  |

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On June 2, 2025, Kymera Therapeutics, Inc. (the "Company") hosted a conference call to discuss the results from the Company's Phase 1 healthy volunteer study of KT-621, an investigational, potentially first-in-class oral STAT6 degrader being developed for the treatment of immuno-inflammatory diseases. A form of the slide presentation is being furnished as Exhibit 99.1 to this Current Report on Form 8-K. The Company undertakes no obligation to update, supplement or amend the materials attached hereto as Exhibit 99.1.

The information in this Item 7.01, including Exhibit 99.1 attached hereto, shall not be deemed "filed" for purposes of Section 18 of the Securities Exchange Act of 1934, as amended, or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, except as expressly set forth by specific reference in such filing.

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| | |
|:---|:---|
| **Item 9.01.** | **Exhibits**  |

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(d) Exhibits

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| | |
|:---|:---|
| **Exhibit<br>No.** | **Description** |
| 99.1 | [Kymera Therapeutics, Inc. slide presentation, dated June 2, 2025, furnished herewith.](d943327dex991.htm) |
| 104 | Cover Page Interactive Data |

---

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#### SIGNATURE
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

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| | | |
|:---|:---|:---|
|  | Kymera Therapeutics, Inc. | Kymera Therapeutics, Inc. |
| Date: June 2, 2025 | By: | /s/ Nello Mainolfi |
|  |  | Nello Mainolfi, Ph.D |

---

## Exhibit 99.1

![](g943327ex99_1p1g1.jpg)

Exhibit 99.1 June 2, 2025 KT-621 / STAT6 Degrader Phase 1 Healthy Volunteer Results Revolutionizing Immunology with Oral Small Molecule Degrader Medicines

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![](g943327ex99_1p2g1.jpg)

Agenda Introduction Justine Koenigsberg Vice President, Investor Relations Revolutionizing Immunology with Oral Medicines Nello Mainolfi, PhD Founder, President and Chief Executive Officer KT-621 Phase 1 Healthy Volunteer Data Jared Gollob, MD Chief Medical Officer Question and Answer Session 2

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![](g943327ex99_1p3g1.jpg)

Forward Looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 and other federal securities laws. These statements include, but are not limited to, implied and express statements about our strategy, business plans and objectives for our programs; plans and timelines for the preclinical and clinical development of our product candidates, including the therapeutic potential, clinical benefits and safety profiles of such product candidates; expectations regarding timing, success and data announcements of ongoing preclinical studies and clinical trials; the preliminary cross-study assessments comparing non-head-to-head clinical data of KT-621 to published data for dupilumab; our ability to initiate new clinical programs, including plans to submit investigational new drug (IND) applications; our ability to deliver additional investigational drugs into the clinic by 2026; the initiation, timing, progress and results of our current and future preclinical studies and clinical trials of our current and prospective product candidates; our plans to develop and commercialize our current and any future product candidates and the implementation of our business model and strategic plans for our business, current; any future product candidates; and our financial condition and expected cash runway into the first half of 2028. All statements other than statements of historical facts contained in this presentation, including express or implied statements regarding our strategy, future financial condition, future operations, projected costs, prospects, plans, objectives of management and expected market growth, are forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as ''anticipate,'' "upcoming," ''assume,'' ''believe,'' ''could,'' ''estimate,'' ''expect,'' ''goal,'' ''intend,'' ''may,'' "milestones," ''objective,'' ''plan,'' ''predict,'' ''potential,'' ''seek,'' ''should,'' ''target,'' ''will,'' ''would'' and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology. We may not actually achieve the plans, intentions or expectations disclosed in our forward-looking statements, and you should not place undue reliance on our forward-looking statements. You should not rely upon forward-looking statements as predictions of future events and actual results or events could differ materially from the plans, intentions and expectations disclosed herein. Any forward-looking statements are based on management's current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-looking statements including, without limitation, risks associated with: the timing and anticipated results of our current and future preclinical studies and clinical trials, supply chain, strategy and future operations; the delay of any current and future preclinical studies or clinical trials or the development of our drug candidates; the risk that the results of prior preclinical studies and clinical trials may not be predictive of future results in connection with current or future preclinical studies and clinical trials, including those for KT-474/SAR-444656, KT-621 and KT-579; the risk that cross-trial comparisons may not be reliable as no head-to- head trials have been conducted comparing KT-621 to dupilumab, and Phase 1 clinical data for KT-621 may not be directly comparable to dupilumab's clinical data due to differences in molecule composition, trial protocols, dosing regimens, and patient populations and characteristics; our ability to successfully demonstrate the safety and efficacy of our drug candidates; the timing and outcome of any interactions with regulatory authorities; obtaining, maintaining and protecting our intellectual property; our relationships with existing and future collaboration partners; the impacts of current macroeconomic and geopolitical events. In addition, any forward-looking statements represent Kymera's views only as of today and should not be relied upon as representing its views as of any subsequent date. Kymera explicitly disclaims any obligation to update any forward-looking statements, except as required by law. No representations or warranties (expressed or implied) are made about the accuracy of any such forward-looking statements. As a result of these risks and others, including those set forth in our filings with the SEC, actual results could vary significantly from those anticipated in this presentation, and our financial condition and results of operations could be materially adversely affected. Certain information contained in this presentation and statements made orally during this presentation relate to or is based on studies, publications, surveys and other data obtained from third-party sources and the Company's own internal estimates and research. No head-to-head trials have been conducted comparing KT-621 to dupilumab. Phase 1 clinical data for KT- 621 may not be directly comparable to dupilumab's clinical data due to differences in molecule composition, trial protocols, dosing regimens, and patient populations and characteristics. Accordingly, cross-trial comparisons may not be reliable. While the Company believes these third-party studies, publications, surveys and other data to be reliable as of the date of the presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, no independent sources have evaluated the reasonableness or accuracy of the Company's internal estimates or research, and no reliance should be made on any information or statements made in this presentation relating to or based on such internal estimates and research. This presentation contains trademarks, trade names and service marks of other companies, which are the property of their respective owners. 3

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![](g943327ex99_1p4g1.jpg)

Revolutionizing Immunology with Oral Medicines Nello Mainolfi, PhD, Founder, President and CEO 4

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![](g943327ex99_1p5g1.jpg)

Kymera: Revolutionizing Immunology with Oral Medicines • Targeted Protein Degradation (TPD) leader • Best-in-industry capabilities in hit finding and optimization of oral degraders • Unique target selection strategy pursuing traditionally undrugged targets in highly validated pathways • Portfolio poised to disrupt conventional treatment paradigms By combining the "right target" with the disruptive potential of TPD, Kymera is delivering oral therapies with biologics-like profiles for the first time in industry with the potential to expand access to millions of patients around the world 5

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![](g943327ex99_1p6g1.jpg)

A Proven Track Record of Reproducible Innovation Productive, Reproducible and Scalable Innovation Engine for High Value Immunology Targets Technology Leader High Productivity Capabilities and know-how to 9 development candidates develop highly potent/specific oral 5 INDs degraders for undrugged proteins Dosed >400 individuals across pipeline Leading I&I Innovation Exceptional Translation First-in-class programs addressing >90% target degradation with historically undrugged and desired tolerability and strong clinical inadequately drugged targets activity across all clinical programs Committed to building a fully-integrated, global, commercial biotech company, 1 capitalized to execute with $775M in cash and runway to the first half of 2028 6

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![](g943327ex99_1p7g1.jpg)

Unique Target Selection Strategy Drives Best-In-Class Pipeline STAT6 Strong Large clinical/ genetic/clinical commercial validation opportunities Undrugged or Clear path to IRF5 inadequately early clinical IRAK4 drugged differentiation targets FOCUS ON FIRST - A ND B E ST - IN - C LA S S O P P OR T U N I TI E S 7

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![](g943327ex99_1p8g1.jpg)

Building a Best-In-Industry Oral Immunology Pipeline Potential Upcoming 2025 1H 2026 Indications Milestones Immunology – Oral Small Molecule Degraders Phase 1 Healthy Volunteer Results AD, Asthma, Ph2b AD Ph1b AD Data: 4Q25 COPD, PN, STAT6 Ph1 HV Ph1b AD Ph2b AD Start: 4Q25 CRSwNP, EoE, KT-621 Ph2b Asthma Ph2b Asthma Start: 1Q26 BP, CSU, others Biomarkers in blood & skin lesions, 28-day efficacy Lupus, IRF5 Ph1 Start: Early 2026 IND Enabling Ph1 Sjögren's, RA, KT-579 IBD, SSc, DM, Program & data disclosure IND Safety, degradation others Partnered with Sanofi/Kymera Opt-In Potential Ph2b HS Ph2b Completion: HS, AD, RA, IRAK4 HS: 1H26 Asthma, 1 2 AD: Mid-2026 KT-474 IBD, others Ph2b AD 8

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![](g943327ex99_1p9g1.jpg)

Immunology: A Large, Underserved Market Oral Degraders with 1 ~160M Total Patients Across Key Immunologic Diseases Biologics-Like Profiles Advanced Therapies: ~5M (3%) Can Disrupt the Immunology Market >$100B >$500B? •∼5M patients (3% of Non-Advanced total diagnosed) are Therapies: •∼ 97% of the ~90M (58%) on systemic advanced diseased population therapies with does not have >$100B in annual access to advanced sales for key I/I • Displace injectable therapies 2 indications biologics • Enormous • Offer a convenient • 2/3 of those untapped market highly effective therapies are Untreated potential advanced therapy to injectable biologics ~62M (39%) the 97% unserved and underserved patients 9

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![](g943327ex99_1p10g1.jpg)

Small Molecule Oral Degraders Can Transform Immunology Potentially Superior Profile to Injectable Biologics and Traditional Small Molecule Inhibitors (SMIs) Biologics can have several limitations, making orals preferred by most patients • Expensive, challenging to prescribe/reimburse 75% • Immunogenicity • Cold storage 1 • Inconvenient and/or painful route In industry surveys , 75% of patients would switch from of administration for patients injectable biologics to oral with similar profile Traditional SMIs insufficiently block pathways, which can limit efficacy 100 SMI 80 70 60 Traditional small molecule Anti IL-23 biologic significantly 50 inhibitors do not allow more effective than TYK2 SMI 40 75% 2 continuous and complete in PsO 30 pathway blockade like degraders 20 32% 10 0 Oral 0 Risankizumab Deucravacitinib Degrader Day 1 Day 2 Day 3 (IL-23 mAb) (TYK2 SMI) 10 Pathway Signaling PASI 90 (%)\* Wk 16

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![](g943327ex99_1p11g1.jpg)

STAT6: An Ideal Immunology Target S T A T 6 T R ANS C R I P T I O N F AC T O R Strong genetic/clinical validation Undrugged or inadequately drugged targets Large clinical/commercial opportunities Clear path to early clinical differentiation 11

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![](g943327ex99_1p12g1.jpg)

S T RO N G G E NE T I C / C L I NI C A L STAT6: Highly Validated Genetically and Clinically VAL ID AT IO N S T A T 6 STAT6 is the Key Signaling Node for IL-4 and IL-13 TRA N S C RI P TI O N • STAT6 is the obligate and specific transcription factor for IL-4/IL-13, F AC T O R which only signal through STAT6 • STAT6 targeting should phenocopy IL-4/IL-13 targeting IL-4/IL-13 Pathway Type I IL-4 Type II IL-4 IL-4/IL-13 Pathway Highly Validated by Dupilumab Receptor Receptor IL-4 IL-4 IL-13 • Dupilumab is approved in 7 indications • AD, Asthma, COPD, PN, CRSwNP, EoE, CSU IL-4Rα γc IL-4Rα IL-13Rα1 • Dupilumab generates >$14B of yearly sales, and is expected to reach 1 $25B by 2030 2 Cytoplasm Strong Genetics Support • Human Gain of Function of STAT6 causes severe allergic disease STAT6 STAT6 KT-621 • Humans with heterozygous Loss of Function are healthy and protected against Th2 inflammation Allergic Th2 Inflammation • STAT6 knock-out mouse is viable, fertile and healthy STAT6 is the only specific STAT6 degradation should lead to Dupilumab-like efficacy in transcription factor responsible for IL-4/13 signaling Th2 diseases with a favorable safety/tolerability profile 12

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![](g943327ex99_1p13g1.jpg)

U N DR U G G E D OR Only STAT6 Degradation Has the Potential to IN AD E Q UAT E L Y D R U GGE D Lead to Dupilumab-Like Pathway Inhibition • STAT6, long pursued immunology "holy-grail" SMI target, has remained undrugged before KT-621 100 • Most oral approaches centered around small molecule inhibitors (SMIs), which have significant limitations • SMIs do not allow continuous and complete pathway blockade because of the direct PK-PD relationship 0 • Only degradation is expected to match dupilumab's Day 1 Day 2 Day 3 pathway blockade with once-a-day oral delivery Oral Degrader 13 Pathway Signaling

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![](g943327ex99_1p14g1.jpg)

L AR G E C L IN IC AL Building a STAT6 Franchise That Will Serve All & C O MME R C I A L O PPO RT U N I T I E S Patients with Th2 Inflammation P a t ie n t 1 N u m be rs DE R M A T OLOG Y 42M AD Total Potential 4.5M CSU Mild Patient Impact: 305K PN 46.5% Only 1% Treated >130M 166K BP with Systemic 1 patients G A S T R OE N T E R OLOG Y Advanced Therapies 1.6M EoE Moderate/Severe Numerous RE S PI RA T O RY indications/ 52.5% therapeutic areas Asthma 55M that are de-risked by dupilumab 34M COPD 1 2.8M CRSwNP >$14B market An oral STAT6 degrader has the potential of transforming the treatment paradigm for Th2 diseases 14

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![](g943327ex99_1p15g1.jpg)

C L E A R PA T H T O KT-621 Development Plan Enables Efficient Path E AR L Y C L IN IC AL D IF F E R E N T IAT IO N to Registration Across All Th2 Diseases Initial Parallel Phase 2b Trials in Moderate/Severe Atopic Dermatitis (AD) and Asthma are Expected to Support Subsequent Phase 3 Trials Across Multiple Dermatology, GI and Respiratory Indications Ph3 AD, Ph2b AD Dose Ranging PN, EoE, BP, CSU Ph3 dose Start in Q4 2025 Ph1 HV Ph1b AD SAD-MAD Single Arm, Open Label Ph3 Asthma, Ongoing ✓ June 2, 2025 Ph2b Asthma COPD, CSRwNP Dose Ranging Data Release Ph3 dose Start in Q1 2026 • Ph3 dose selected for AD has • Safety and tolerability • Dosing for 28 days • Efficacy and safety in potential to be used for other two initial Th2 diseases • STAT6 degradation • Biomarkers in blood derm/GI indications, such as PN, and skin lesions • Ph3 dose selection for EOE, BP, and CSU • Th2 biomarkers franchise • Ph3 dose selected for asthma has • Clinical activity potential to be used for other respiratory indications, such as COPD and CRSwNP 15

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![](g943327ex99_1p16g1.jpg)

KT-621: Compelling Preclinical Package Excellent Preclinical Efficacy Robust Degradation Highly Potent Exquisite Selectivity KT-621 can degrade STAT6 90% STAT6 degradation leads to Full inhibition of IL-4/IL-13 pathways Complete STAT6 degradation selectivity in all relevant tissues in comparable or superior in vivo efficacy more potent than dupilumab in human PBMC at 100xDC 90 non-human primates (NHP) to dupilumab in asthma models IL-4 Induced TARC Release in TARC (CCL17) Reduction in Lungs STAT6 Degradation in NHP Tissues Human PBMC Post 14 Days of KT-621 10 mpk QD IC 50 Oral Dosing KT-621 62 pM 0 Dupilumab 194 pM 4 -50 Reduction in Lung Goblet Cell Metaplasia Concentration (pM) IL-13 Induced Periostin Release in 2 Human Bronchial Smooth Muscle Cell IC 50 KT-621 24 pM Dupilumab 637 pM -100 0 -2 0 2 Log2(Fold-Change) Concentration (pM) Safety: Well tolerated in multiple preclinical species and safety studies at concentrations 40-fold above efficacious dose 16 -Log10(p-Value) Percentage to DMSO Percentage to DMSO STAT6% Degradation vs Pre Dose Goblet Cell Score TARC (pg/ml)

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![](g943327ex99_1p17g1.jpg)

Phase 1 Healthy Volunteer Exceeded Study Objectives Clinical Data Continues to Support a Dupilumab-like Profile KT-621 Healthy Volunteer KT-621 Healthy Volunteer Endpoint Objectives Data STAT6 Degradation in Blood 90%+ Complete STAT6 Degradation in Skin 90%+ Complete Well tolerated 16-fold above the Well tolerated Safety dose with >90% degradation; at 90%+ degradation No SAEs; No TRAEs >1 subject Robust inhibition of several Dupi-like profile Th2 Biomarkers biomarkers, comparable/superior (non dose-dependent TARC reduction) to published dupilumab data 17

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![](g943327ex99_1p18g1.jpg)

Phase 1 Healthy Volunteer Data Surpass Target Product Profile (TPP) and Underscore Significant Potential of KT-621 Conclusions / Next Steps Phase 1 HV Goals Exceeded ü Potent Degradation • KT-621 profile surpasses Kymera's TPP with compelling preclinical profile human translation above expectations • >90% STAT6 degradation in blood in all doses above 1.5 mg • We believe the results derisk program and continue to • Complete STAT6 degradation achieved in both blood and validate KT-621's oral, biologics-like profile skin in all doses ≥50 mg • Proven biology of IL-4/IL-13 pathway, and clearly ü Encouraging Th2 Biomarker Impact defined market development path, create a unique and • Results in line or superior to published data for compelling opportunity dupilumab, with strong TARC and Eotaxin-3 reductions • Study informs continued development, including ü Excellent Tolerability ongoing Phase 1b in AD and upcoming Phase 2b studies • KT-621 was well-tolerated with a safety profile in AD and Asthma undifferentiated from placebo 18

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![](g943327ex99_1p19g1.jpg)

KT-621/STAT6 Degrader: Dupilumab-like Activity in a Pill Phase 1 Healthy Volunteer Data Jared Gollob, MD, Chief Medical Officer 19

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![](g943327ex99_1p20g1.jpg)

Agenda • Trial Description • Demographics • Pharmacokinetics (PK) • SAD Degradation • MAD Degradation • Th2 Biomarkers • Safety 20

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![](g943327ex99_1p21g1.jpg)

KT-621: Phase 1a SAD and MAD Healthy Volunteer Trial Randomized, Double-blind, Placebo-controlled SAD and MAD in 118 Healthy Volunteers Part B Part A Primary Multiple Ascending Dose Single Ascending Dose (MAD) (SAD) • Safety & tolerability of 14x daily doses escalating single and multiple doses of KT-621 800 mg 200 mg 400 mg 100 mg Secondary 200 mg 50 mg • Pharmacokinetic measures 75 mg 25 mg 25 mg 12.5 mg 6.25 mg 1.5 mg Exploratory Total 48 Total 70 • STAT6 protein levels in blood Healthy Volunteers Healthy Volunteers\* (SAD/MAD) and skin (MAD) 8 per cohort 12 per cohort • Th2 biomarkers (MAD) (6:2 KT-621:Placebo) (9:3 KT-621:Placebo) 21

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![](g943327ex99_1p22g1.jpg)

SAD/MAD Demographics Generally Well-Balanced Across Placebo and Treatment Arms SAD 1-6: SAD 1-6: MAD 1-6: MAD 1-6: PBO KT-621 PBO KT-621 (n=12) (n=36) (n=18) (n=52) Gender, n (%) Female 7 (58.3) 11 (30.6) 0 5 (9.6) Male 5 (41.7) 25 (69.4) 18 (100) 47 (90.4) Age, years, median (range) 34.5 (20, 50) 32.0 (21, 43) 34.0 (23, 53) 32.5 (19, 52) Ethnicity, n (%) Hispanic or Latino 1 (8.3) 9 (25.0) 4 (22.2) 14 (26.9) Non-Hispanic or Latino 11 (91.7) 27 (75.0) 14 (77.8) 38 (73.1) Race, n (%) White 9 (75.0) 18 (50.0) 10 (55.6) 29 (55.8) Black or African American 2 (16.7) 12 (33.3) 6 (33.3) 17 (32.7) Asian 0 0 2 (11.1) 3 (5.8) 0 1 (2.8) 0 0 Native Hawaiian or Pacific Islander 0 0 0 1 (1.9) American Indian or Alaska Native Mixed/Other 1 (8.3) 5 (13.9) 0 2 (3.8) 22

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![](g943327ex99_1p23g1.jpg)

SAD & MAD KT-621: Favorable PK Profile After Single and Multiple Dosing Steady-State (Day 14) Single Dose PK Profiles 6.25 mg SD n=6 1.5 mg QD n=9 Multi-Dose PK Profiles 25 mg SD n=6 12.5 mg QD n=7 75 mg SD n=6 25 mg QD n=9 200 mg SD n=6 50 mg QD n=9 400 mg SD n=6 100 mg QD n=9 800 mg SD n=6 200 mg QD n=9 LLOQ\* LLOQ\* Time (Hours) Time (Hours) • Rapid absorption with median t of 2-4 hours and mean half-life of 9-36 hours max • Generally dose-proportional increase in exposure after single and multiple doses with low-moderate variability • Steady-state achieved by Day 4 of once daily dosing 23 KT-621 Plasma Concentration (ng/mL) Mean (±SD) KT-621 Plasma Concentration (ng/mL) Mean (±SD)

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![](g943327ex99_1p24g1.jpg)

SAD Single Doses of KT-621 Achieved Rapid, Deep and Prolonged STAT6 Degradation in Blood 1 Absolute STAT6 Levels Mean Percent Change from Baseline in STAT6 Placebo n=12 Placebo n=12 1.5 100 6.25 mg SD n=6 6.25 mg SD n=6 25 mg SD n=6 25 mg SD n=6 75 mg SD n=6 75 mg SD n=6 50 200 mg SD n=6 200 mg SD n=6 1.0 400 mg SD n=6 400 mg SD n=6 800 mg SD n=6 800 mg SD n=6 0 0.5 -50 LLOQ\* 0.0 -100 0hr 4hr 8hr 24hr 48hr D4 D5 D10 D14 0hr 4hr 8hr 24hr 48hr D4 D5 D10 D14 Time/Day\*\* Time/Day\*\* • Maximal degradation seen as quickly as 4 hours after single dose • Robust degradation maintained as long as 4 days after single dose with recovery by Day 14 • Multiple subjects with STAT6 levels below LLOQ at doses of 75 mg or greater 24 Mean (±SE) Abs STAT6 (fmol/µg pep) Mean (±SE) Percent Change from Baseline in STAT6

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![](g943327ex99_1p25g1.jpg)

SAD Single Dose Administration of KT-621 Achieved >90% STAT6 Degradation in Blood Across All Dose Levels >95% Mean STAT6 Degradation Achieved at Doses of 75 mg or Greater Placebo 20 6.25 mg SD 0 25 mg SD -20 75 mg SD 200 mg SD -40 400 mg SD -60 800 mg SD -80 -100 4 8 24 4 8 24 4 8 24 4 8 24 4 8 24 4 8 24 4 8 24 Hours Post Dose Mean % STAT6 Change N 4hr 8hr 24hr Placebo 12 21% 17% -10% 6.25 mg 6 -80% -93% -87% 25 mg 6 -82% -94% -94% 75 mg 6 -96% -97% -96% 200 mg 6 -97% -98% -97% 400 mg 6 -96% -97% -96% 800 mg 6 -97% -98% -98% • At doses ≥75 mg, >95% mean STAT6 degradation was achieved with STAT6 levels below LLOQ in multiple subjects • p < 0.0001 for all comparisons (KT-621 vs. Placebo) 25 Mean (±SE) Percent Change from Baseline in STAT6

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![](g943327ex99_1p26g1.jpg)

MAD Multiple Daily Doses of KT-621 Rapidly (8hr) Achieved Complete STAT6 Degradation in Blood 1 Mean Absolute STAT6 Levels Mean Percent Change from Baseline in STAT6 200 Placebo n=18 Placebo n=18 150 1.5 mg QD n=9 1.5 mg QD n=9 100 12.5 mg QD n=7 12.5 mg QD n=7 1.0 50 25 mg QD n=9 25 mg QD n=9 0 50 mg QD n=9 0 50 mg QD n=9 100 mg QD n=9 100 mg QD n=9 200 mg QD n=9 200 mg QD n=9 0.5 -100 LLOQ\* 0.0 0 hr 8hr 24hr D4 D7 D14 D18 D28 D38 0 hr 8hr 24hr D4 D7 D14 D18 D28 D38 ON TREATMENT ON TREATMENT Time/Day\*\* Time/Day\*\* • Robust STAT6 degradation observed at first time point measured (8hr) for all doses above 1.5 mg • Steady-state maximum degradation achieved as early as 8hr post-first dose with recovery starting at 4 days post-last dose • Most subjects with STAT6 levels below LLOQ at doses of ≥50 mg 26 Mean (±SE) STAT6 (fmol/µg pep) Mean (±SE) Percent Change from Baseline in STAT6

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MAD Multiple Daily Doses of KT-621 Achieved >90% STAT6 Degradation in Blood at All Dose Levels Above 1.5 mg Complete Degradation Achieved at Doses of 50 mg or Greater 100 Placebo n=18 1.5 mg QD n=9 12.5 mg QD n=7 25 mg QD n=9 0 50 mg QD n=9 100 mg QD n=9 200 mg QD n=9 -100 D1, 8hrD7 D14 D1, 8hrD7 D14 D1, 8hrD7 D14 D1, 8hrD7 D14 D1, 8hrD7 D14 D1, 8hrD7 D14 D1, 8hrD7 D14 Time Post First Dose Mean % STAT6 Change Day 1, 8hr Mean % STAT6 Change Day 7 Mean % STAT6 Change Day 14 Placebo 43% 44% 56% 1.5 mg -34% -67% -68% 12.5 mg -84% -90% -92% 25 mg -94% -95% -94% 50 mg -94% -94% -92% 100 mg -98% -97% -98% 200 mg -97% -97% -94% • At doses ≥50 mg STAT6 Levels are below LLOQ for the majority subjects at day 14 • p < 0.0001 for all comparisons (KT-621 vs. Placebo) 27 Mean (±SE) Percent Change from Baseline in STAT6

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MAD Multiple Daily Doses of KT-621 Achieved Complete STAT6 Degradation in Skin 1 Mean Absolute STAT6 Levels Mean Percent Change from Baseline in STAT6 100 0.3 Placebo n=17 Placebo n=17 1.5 mg QD n=7 1.5 mg QD n=7 12.5 mg QD n=7 12.5 mg QD n=7 25 mg QD n=8 25 mg QD n=8 0.2 50 mg QD n=9 50 mg QD n=9 100 mg QD n=9 100 mg QD n=9 0 200 mg QD n=9 200 mg QD n=9 0.1 -100 LLOQ\* 0.0 1 7 14 28 1 7 14 28 ON TREATMENT ON TREATMENT Day\*\* Day\*\* • Baseline skin STAT6 levels 5-fold lower than peripheral blood mononuclear cells (PBMC) • Steady-state maximum STAT6 degradation achieved by Day 7 at doses >1.5 mg with recovery observed 14 days post-last dose 28 Mean (±SE) STAT6 (fmol/µg pep) Mean (SE±) Percent Change from Baseline in STAT6

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MAD Multiple Daily Doses of KT-621 Achieved Complete STAT6 Degradation in Skin at All Doses ≥50 mg Placebo n=17 0 1.5 mg QD n=7 12.5 mg QD n=7 25 mg QD n=8 -50 50 mg QD n=9 100 mg QD n=9 200 mg QD n=9 -100 7 14 7 14 7 14 7 14 7 14 7 14 7 14 Day Mean% Change in STAT6 Mean % Change in STAT6 Day 7 Day 14 Placebo -11% -8% 1.5 mg -24% -48% 12.5 mg -93% -92% 25 mg -89% -88% 50 mg -96% -96% 100 mg -93% -95% 200 mg -97% -97% • At doses ≥50 mg, ≥95% mean STAT6 degradation was achieved with STAT6 levels below LLOQ in multiple subjects • p < 0.0001 for all comparisons (KT-621 vs. Placebo) 29 Mean (±SE) Percent Change from Baseline in STAT6

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Th2 Biomarkers 30

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TARC, IgE, and Eotaxin-3: Validated Biomarkers of Th2 Biology 1 Not Typically Elevated in HV Subjects Without Th2-Driven Disease TARC (CCL17) Immunoglobulin E (IgE) Eotaxin-3 (CCL26) • TARC is the chemokine responsible • IgE activates mast and basophil cells to • The chemokine responsible for chemotaxis of CCR3-expressing for chemotaxis of CCR4-expressing T produce allergic inflammatory mediators cells (e.g., Th2) to sites of inflammation (e.g., IL-4 and IL-13) inflammatory cells (e.g., eosinophils) to sites of inflammation • TARC is a validated biomarker in • IL-4 promotes B cell class switching which patients for suppression of Th2 driven produces more IgE • Eotaxin-3 is a highly specific inflammatory responses downstream cytokine of IL-4/IL-13 • IgE half-life is estimated to be 3 days; pathway • Constitutive normal levels of TARC however, turnover of IgE producing B cells might be partially dependent on and long-lived plasma cells is longer • Only assessed in dupilumab patient IL-4Rα studies • Assessed in dupilumab healthy volunteer • Assessed in dupilumab healthy studies volunteer studies 31

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TARC and IgE Assessment in Dupilumab Healthy Volunteer Study Dupilumab Decreased TARC up to 35% in a High Variability and Minimal Changes Non-Dose Dependent Manner in Healthy in IgE after 1-4 Week Volunteers Days Days Li et al. Clinical Pharmacology Drug Development (2020) • No meaningful changes of IgE in HV within first week with • Non-dose dependent TARC reduction was observed in modest maximal effect of ∼15% after 1 month the study in some but not all doses • In patients where baseline levels of IgE are higher, IgE • 300 mg SC dose gave max median reduction of ∼35% reduction is minimal within first 2-4 weeks; months are • Assay window likely very small given that baseline is often required to see robust reduction of IgE in patients within normal range with Th2 diseases 32 Median % Change from Baseline in TARC Median % Change from Baseline in IgE

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MAD Multiple Daily Doses of KT-621 Achieved Up to 37% Median TARC Reduction Median Percent Change from Mean Percent Change from 1 1 Baseline in Serum TARC Baseline in Serum TARC Median % Mean % Placebo n=18 Day 14 Change Change in TARC in TARC 1.5 mg QD n=9 20 20 12.5 mg QD n=7 Placebo -13% 1% 25 mg QD n=8 50 mg QD n=8 1.5 mg -15% -15% 100 mg QD n=9 0 0 200 mg QD n=9 12.5 mg -36% -34% 25 mg -21% -2% -20 -20 50 mg -37% -39% 100 mg -11% -12% -40 -40 200 mg -31% -23% 1 4 7 14 28 1 4 7 14 28 ON TREATMENT ON TREATMENT Day\* Day\* • TARC reduction achieved in all KT-621 doses within the first 14 days 2 • Baseline TARC levels in line with dupilumab HV study 33 Percent Change from Baseline in TARC

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MAD High Variability and Minimal Changes in IgE with Multiple Daily Oral Doses of KT-621 Median % Change from Mean % Change from 1 1 Baseline in IgE Median% Mean % Baseline in IgE Day 14 Change Change Placebo n=18 10 10 In IgE In IgE 1.5 mg QD n=9 12.5 mg QD n=7 Placebo -13% -8% 25 mg QD n=8 50 mg QD n=8 1.5 mg -12% -13% 0 0 100 mg QD n=8 200 mg QD n=9 12.5 mg -7% -10% 25 mg -8% -7% -10 -10 50 mg -5% -5% 100 mg -11% -11% 200 mg -2% -1% -20 -20 1 4 7 14 28 1 4 7 14 28 ON TREATMENT ON TREATMENT Day\* Day\* • Results consistent with dupilumab effect on IgE in healthy volunteers 2 • Baseline IgE levels in line with dupilumab HV study 34 Percent Change from Baseline in IgE

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MAD Multiple Daily Doses of KT-621 Achieved Up to 63% Median Eotaxin-3 Reduction Median Percent Change from Mean Percent Change from 1 1 Baseline in Serum Eotaxin-3 Baseline in Serum Eotaxin-3 Median % Mean % Day 14 Change Change Placebo n=18 in Eotaxin-3 in Eotaxin-3 20 20 1.5 mg QD n=9 12.5 mg QD n=7 Placebo -4% -7% 25 mg QD n=8 0 0 50 mg QD n=8 1.5 mg -28% -26% 100 mg QD n=8 200 mg QD n=9 -20 -20 12.5 mg -58% -55% 25 mg -62% -57% -40 -40 50 mg -55% -57% -60 -60 100 mg -63% -50% 200 mg -42% -41% -80 -80 1 4 7 14 28 1 4 7 14 28 ON TREATMENT ON TREATMENT Day\* Day\* • Dupilumab reduced serum Eotaxin-3 by 38% in asthma and 51% in CRSwNP patients 2, 3 at 52 weeks of treatment in Phase 3 studies (no data in healthy volunteers) 35 Percent Change from Baseline in Eotaxin-3

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SAD & MAD Healthy Volunteer SAD/MAD Safety Summary KT-621 Well Tolerated Across All Doses Evaluated Undifferentiated from Placebo TRAEs by Preferred Term: SAD Cohort • No SAEs SAD 1-6: SAD 1-6: AE Term (severity) PBO KT-621 • No Severe AEs (n=12) (n=36) Headache (mild) 1 (8.3%) 0 • No dose dependent pattern in the TEAEs • No treatment related AE reported in >1 TRAEs by Preferred Term: MAD Cohort participant MAD 1-6: MAD 1-6: • No related TEAEs leading to AE Term (severity) PBO KT-621 discontinuation (n=18) (n=52) Nausea (mild) 1 (5.6%) 0 • No clinically relevant changes in vital Asthenia (mild) 0 1 (1.9%) signs, laboratory tests, and ECGs 36

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Phase 1 Healthy Volunteer Data Surpass Target Product Profile (TPP) and Underscore Significant Potential of KT-621 Conclusions / Next Steps Phase 1 HV Goals Exceeded ü Potent Degradation • KT-621 profile surpasses Kymera's TPP with compelling preclinical profile human translation above expectations • >90% STAT6 degradation in blood in all doses above 1.5 mg • We believe the results derisk program and continue to • Complete STAT6 degradation achieved in both blood and validate KT-621's oral, biologics-like profile skin in all doses ≥50 mg • Proven biology of IL-4/IL-13 pathway, and clearly ü Encouraging Th2 Biomarker Impact defined market development path, create a unique and • Results in line or superior to published data for compelling opportunity dupilumab, with strong TARC and Eotaxin-3 reductions • Study informs continued development, including ü Excellent Tolerability ongoing Phase 1b in AD and upcoming Phase 2b studies • KT-621 was well-tolerated with a safety profile in AD and Asthma undifferentiated from placebo 37

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