Document:

Exhibit 10.2

 

	 	REDACTED
	 	*Certain identified information has been excluded from the exhibit because it is both: (i) not material and (ii) would be competitively harmful if publicly disclosed.*

 

MEMORANDUM OF UNDERSTANDING

 

This Memorandum of Understanding (“MOU”)
is made as of July 28, 2018 (the “Effective Date”), by and between Yissum Research Development Company of the
Hebrew University of Jerusalem Ltd. of Hi Tech Park, Edmond J. Safra Campus, Givat Ram, Jerusalem 91390, Israel (“Yissum”),
of the first part and Scopus BioPharma Israel Ltd., 22 Joseph Rivlin Street, Jerusalem 9424018 (the “Company”);
of the second part (Yissum and the Company collectively the “Parties”; each of Yissum and the Company, individually,
a “Party”).

 

WHEREAS, Yissum is interested in
receiving funding and the Company is willing to fund the conduct of a feasibility study led by Dr. Dmitry Tsvelikhovsky (the “Researcher”)
and his teams at the Hebrew University of Jerusalem (the “University”), for the project entitled “A
New Synthesis Protocol for Cannabinoid Molecules” (the “Project”). The feasibility study will be
carried out, under the Company’s sponsorship and supervision, by the Researcher and his teams at the University, in accordance
with the study program set forth in Appendix A (the “Study”), annexed to this Agreement and forming an integral
part of this MOU;

 

AND WHERAS, the Company wishes,
subject to its sole discretion, to obtain a license to the Results (as such term is defined below) in the Field (as such term is
defined below) in accordance with the agreed upon commercial terms set forth in Appendix B; and all subject to the terms and conditions
of this MOU.

 

NOW, THEREFORE, in consideration
of the foregoing and of the mutual covenants set out herein, and other good and valuable consideration, the Parties hereby agree
as follows:

 

		1.	The Study

 

		1.1	The Company
                                         hereby undertakes to finance performance of the Study for a period of two years (“Study
                                         Period”) in accordance with the Study Program or any amendment thereof. Such
                                         financing shall be, subject to any earlier termination of the Study pursuant to section
                                         1.2, below, in an amount of NIS 749,249 (Seven Hundred Forty Nine Thousand and Two Hundred
                                         and Forty Nine NIS) plus VAT (inclusive of overhead) (the “Study Fee”)
                                         payable as follows: (i) on September 1st 2018 [                                                                                                                                                                    ]
                                         plus VAT and (ii) on the six (6) months anniversary of the Effective Date, [                                                                                  ]

 

		1.2	The Study shall be conducted by and under the supervision
of the Researcher. Should the Researcher be unable to complete the Study for any reason, Yissum shall notify the Company in writing
of the identity of a replacement researcher along with such documentation to support such replacement researcher’s qualifications.
If the replacement researcher is not acceptable to the Company in its sole discretion, the Company upon written notice to Yissum
delivered within 30 days of notice of the proposed replacement researcher shall have the right to terminate for convenience the
Study, provided that (i) no monies paid to Yissum for the Study will be refundable other than amounts paid in advance for the
costs of the Study which have not yet been expended or obligated; and (ii) the Company shall be responsible for the payment of
any accrued fees and expenses due to Yissum based on work duly performed up to the date of termination and those irrevocable commitments
entered into by Yissum prior to having received the Company’s written notice of termination. For the avoidance of any doubt,
the Company shall not be required to pay any balance of the Study Fee to Yissum other than set forth in this Section 1.2.

 

		1.3	At the end
                                         of the Study Period, Yissum shall present the Company with a written report from the
                                         Researcher summarizing the results of the Study during the Study Period (the “Scientific
                                         Report”). In addition, Yissum shall provide updates of its progress no less
                                         often than quarterly and shall respond to the Company’s reasonable requests for
                                         progress information from time to time.

 

    	 

     

    

 

		2.	Notice.
                                         At any time during the Study Period until sixty (60) days following receipt by the Company
                                         of the Scientific Report (the “Notice Period”), the Company shall
                                         have the right to deliver written notice to Yissum (the “Notice”)
                                         as to whether the Company (on its own or in conjunction with a partner of the Company),
                                         desires to commercialize the inventions, patents, patent applications, information, material,
                                         results, devices, and/or know-how created, generated or reduced to practice in the course
                                         of or arising from the performance of the Study (the “Results”) in
                                         the Field. For the purpose of this Agreement, “Field” shall mean pain
                                         and anesthesia.

 

		3.	Ownership of the Results. Yissum shall own
all Results (including any new intellectual property and know-how developed by, or under the direction of, the Researcher before
and during the Study).

 

		4.	Confidentiality.
                                         During the Study Period and through the end of the Negotiation Period or the execution
                                         of the License Agreement, whichever occurs first, the Company and Yissum shall safeguard
                                         as confidential all non-public information regarding the Study and the Results (“Confidential
                                         Information”) and shall not use or disclose the Results except for purposes
                                         of evaluating the possibility of commercializing the Results. The Company shall ensure
                                         that every third party to whom it has disclosed any Confidential Information shall comply
                                         with the foregoing confidentiality and non-disclosure obligations. The Company shall
                                         not mention the name of the University, Yissum or the Researcher unless required by law
                                         or in connection with prosecuting and/or maintaining the Results Patents (as defined
                                         below), in any manner or for any purpose in connection with this Agreement or any matter
                                         relating to the Study, without obtaining the prior written consent of Yissum which shall
                                         not be unreasonably withheld; provided, however, no such consent shall be required if
                                         such disclosure is undertaken in connection with the Company’s capital raising
                                         efforts or for public reporting requirements.

 

		5.	License.
                                         If the Company provides the Notice within the Notice Period, the Parties shall have a
                                         period ending one hundred eighty (180) after the end of the Notice Period (“Negotiation
                                         Period”) for Yissum to exclusively negotiate a license agreement with the Company
                                         upon the commercial terms and conditions set forth in Appendix B, which forms an integral
                                         part of this MOU, and on additional commercial and other terms and conditions (the “License
                                         Agreement”). If such negotiations, which the Parties agree to undertake in
                                         good faith, do not result in the execution of a License Agreement within the Negotiation
                                         Period, either of the Parties shall have the right to withdraw from such negotiations.
                                         Yissum shall thereafter have the right to extend a license to any third party. Upon extension
                                         of such license and provided that such license generates license consideration, Yissum
                                         shall pay to the Company twenty percent (20%) of the “Net Proceeds”
                                         (as such term is defined below) actually received by Yissum from such license to a third
                                         party, until such time as the Company shall have received, in aggregated, [         ]
                                         of the Study Fee and all patent prosecution costs that Company may have advanced hereunder
                                         (the “Reimbursement”).

 

For the purpose of this section, “Net
Proceeds” means royalties, sublicense consideration or license milestone consideration actually received by Yissum in
respect of such license with a third party (excluding payments for the supply of services or materials or for patent expenses)
after deduction of: (a) all costs, fees and expenses incurred by Yissum in connection with such license (including patent costs
not reimbursed as aforesaid, all out-of-pocket attorney’s fees and expenses and other direct costs and expenses in connection
with the negotiation and execution of such license); and (b) amounts, if any, required by Yissum to pay governmental or regulatory
authorities (including the Israel Innovation Authority) by virtue of any funding, support or assistance received via programs or
collaborations, unless Yissum has already been reimbursed for such governmental/regulatory authority payments by the third party
licensee.

 

    	2

     

    

 

		6.	No Notice. In the event that Yissum does
not receive the Notice during the Notice Period, neither Yissurn nor the Researcher shall have any further obligations towards
the Company with respect to the Results or the Project and shall be entitled, at its discretion, to freely disclose, exploit and
commercialize the Results. In addition, the Company’s obligations of confidentiality and non-disclosure (regarding the Study
and the Results) described in Section 4 shall continue in effect until the particular Confidential Information enters the public
domain through no breach thereof by the Company or its representatives.

 

		7.	No-Shop Period. In consideration for the
Company agreeing to fund the conduct of the Study as provided herein, Yissum hereby gives the Company a “No-Shop”
undertaking obligating Yissum during a period from the Effective Date until the later of (a) the end of the Notice Period; and
(b) the end of the Negotiation Period, if applicable (the “No-Shop Period”), not to engage in any discussions
or negotiations with any third party (except for a partner of the Company) for the commercial use of the Results (including any
new intellectual property and know-how conceived of and generated during the Study). In the event that Yissum does not receive
the Notice by the end of the Notice Period stating that the Company desires to commercialize the Results as aforesaid, then the
No-Shop Period will automatically terminate at the end of the Notice Period.

 

		8.	Patents. As of the Effective Date, the Company
shall be responsible for ongoing costs in connection with the filing, prosecution and maintenance of any patents arising from
the Results (the “Results Patents”). If a License Agreement is not executed, all costs advanced by Company
shall be promptly reimbursed to the Company.

 

		9.	Publication. Yissum, subsequent to the execution
of this Agreement, shall ensure that during the term of this Agreement no publication in writing of any Results in scientific
journals, or orally at scientific conventions, are published by it or the Researcher unless Yissum has taken the necessary steps
to protect any patentable invention being disclosed in such proposed publication or scientific conventions and has obtained the
prior written consent of the Company which shall not be unreasonably withheld.

 

		10.	Liability and Indemnity.

 

		10.1	YISSUM MAKES NO WARRANTIES OF ANY KIND WITH RESPECT TO
THE STUDY. IN PARTICULAR, YISSUM MAKES NO WARRANTIES THAT ANY RESULTS OR INVENTIONS WILL BE ACHIEVED BY THE STUDY, OR THAT THE
RESULTS, IF ANY, ARE OR WILL BE COMMERCIALLY EXPLOITABLE OR THAT THE RESULTS PATENTS, IF ANY, WILL NOT INFRINGE ANY PATENT, COPYRIGHT,
TRADEMARK OR OTHER RIGHTS OF ANY THIRD PARTY. YISSUM SHALL HAVE NO LIABILITY WHATSOEVER TO THE COMPANY OR TO ANY THIRD PARTY FOR
OR ON ACCOUNT OF ANY INJURY, LOSS, OR DAMAGE, OF ANY KIND OR NATURE, SUSTAINED BY THE COMPANY OR BY ANY THIRD PARTY, FOR ANY DAMAGE
ASSESSED OR ASSERTED AGAINST THE COMPANY, OR FOR ANY OTHER LIABILITY INCURRED BY OR IMPOSED UPON THE COMPANY OR ANY OTHER PERSON
OR ENTITY, ARISING OUT OF OR IN CONNECTION WITH OR RESULTING FROM THE USE OF THE RESULTS.

 

		10.2	The Company shall be liable for any loss, injury or damage
whatsoever caused to its employees or to any person acting on its behalf or to the employees of Yissum, the University, or to
any person acting on their behalf, or to any third party by reason of the Company’s acts or omissions pursuant to this Agreement
or by reason of any use made of the Results.

 

    	3

     

    

 

		10.3	The Company undertakes to compensate, indemnify, defend
and hold harmless Yissum and the University, or any person acting on their behalf, including, without limitation, any of their
employees or representatives (the “Indemnitees”) against any liability including, without limitation, product
liability, damage, loss or expenses, including reasonable legal fees and litigation expenses, incurred by or imposed upon the
Indemnitees by reason of its acts or omissions or which derive from the Company’s use of the Results.

 

		11.	Termination of the Agreement. In addition
to the termination right in favor of Company set forth in Section 1.2, this Agreement shall automatically terminate upon the occurrence
of the earlier of: (i) the Company fails to provide Yissum with a Notice before the end of the Notice Period; or (ii) the Company
and Yissum fail to execute a License Agreement by the end of the Negotiation Period. In addition, Yissum shall be entitled to
terminate this Agreement upon fourteen (14) days prior written notice to the Company in the event of unauthorized early termination
by the Company of the Study or failure to pay any part of the Study Fee as set forth in Section 1.1 above within fourteen (14)
days of receipt of written notice from Yissum to the Company advising that any payment is past due. The termination of this Agreement
for any reason shall not release the Company from its obligation to carry out any financial or other obligation which it was liable
to perform prior to the Agreement’s termination.

 

		12.	Notices. All notices and communications pursuant
to this Agreement shall be made in writing and sent by registered mail or overnight delivery service to or served at the following
addresses:

 

Yissum Research Development Company
of the Hebrew University of Jerusalem Ltd., POB 39135, Jerusalem 91390, Israel, Attn: Ariela Markel.

 

Scopus BioPharma Israel Ltd., c/o
Scopus BioPharma Inc., 420 Lexington Avenue, Suite 300, New York, New York 10170, Attn: Robert J. Gibson.

 

or such other address furnished in accordance
with the aforesaid by one Party to the other. Any notice sent as aforesaid shall be deemed to have been received 4 days after being
posted by registered mail, or 1 day after personal service, as the case may be.

 

		13.	Governing Law; Jurisdiction. Each Party agrees
that this MOU shall be governed exclusively by Israeli law without application of any conflict of law principles, and jurisdiction
shall be granted to the competent courts in Jerusalem, Israel and each party irrevocably submits to the jurisdiction of such courts.

 

IN WITNESS WHEREOF, the Parties have caused
this MOU to be executed by their duly authorized representatives effective as of the date set forth above.

 

	YISSUM RESEARCH AND DEVELOPMENT COMPANY OF THE HEBREW UNIVERSITY OF JERUSALEM LTD.	 	SCOPUS BIOPHARMA ISRAEL LTD.
	 	 	 	 	 
	By:	/s/ Ariela Markel	 	By:	/s/ Morris Laster
	 	 	 	 	 
	Name:	Ariela Markel, M.Sc., MBA	 	Name:	Morris Laster MD
	 	 	 	 	 
	Title:	VP Licensing, Biotechnology	 	Title:	CEO

 

	/s/ Yaron Daniely	 	 
	Dr. Yaron Daniely	 	 
	CEO of Yissum	 	 

 

    	4

     

    

 

I the undersigned, Dr. Dmitry Tsvelikhovsky,
have reviewed, am familiar with and agree to all of the above terms and conditions. I hereby undertake to cooperate fully with
Yissum in order to ensure its ability to fulfill its obligations hereunder, as set forth herein.

 

	 	/s/ Dmitry Tsvelikhovsky	 	2/8/2018	 
	 	Dr. Dmitry Tsvelikhovsky	 	Date signed	 

 

    	5

     

    

 

Appendix A

 

Study Program

LINE – 1: Synthesis of new derivatives
of CBG and THCV

 

Aims:

		-	Synthesis of CBG and THCV on gram-scale from commercially
available materials (based on published protocols)

		-	Synthesis of CBG and THCV structural analogues (according
to the proposed strategy)

 

Milestones:

 

 

Project execution: The laboratory of synthetic medicinal
chemistry at the School of Pharmacy HUJI.

The space consists of a total of ~80 square meters. The lab
space includes:

1. Six chemical fume hoods (each equipped with Schlenk-line
system); 2. Chromatography setup: GC (equipped with FID detector) and ISQ EI-Single Quadruple Mass Spectrometer; 3. Inert atmosphere
workstation: Glove box and Solvent Purification System; 4. Chemical refrigerators; 5. Rotovapors; 6. Balances; 7. Oven; 8. Desiccators,
etc.

 

Manpower: 1 Postdoc

 

Projected duration[              ]

 

	I - Synthesis of THCV from commercially available precursors

 

Synthetic Flow: 1 ® 2a+2b (separation + purification);
2b ® 3 (purification); 4 + 5 ® 6 (purification); Deprotection of 6 (purification); 3 + 6 ® THCV (purification).

 

 

    	6

     

    

 

 

Known derivatives of THCV

 

 

	II - Synthesis of new THCV derivatives (Proposal)

 

Two types of derivatization strategies
will be applied: a) post-synthetic modification (the synthesized THCV will be employed for further structural changes),
and b) in-sequence modification, where modified starting materials (building blocks) [                                              ]

 

 

Overall: 7-10 new compounds are proposed

 

    	7

     

    

 

 

	III - Synthesis of CBG from commercially available precursors

 

Flow: 11 + 12 ® CBG (purification)

 

The protection-deprotection of 11 and 13 might
be required:

 

 

	IV - Synthesis of new CBG derivatives (proposal)

 

The derivatization of CBG will be performed using post-synthetic
strategy.

Two derivatives [                            ]
will be prepared as demonstrated below:

 

 

Overall: 2-4 new compounds are proposed

 

    	8

     

    

 

	Budget

 

Request for 50% upon signing and additional half way 50% after
3 months.

 

 

    	9

     

    

 

 

LINE – 2: Fusion of the CBD molecule with market drugs
[                                           ]

 

Aim:

 

		-	Integration
                                         of the CBD scaffold with market drugs [                                           ]

 

 

Milestones:

 

 

The solubility of the newly designed “super-drugs”
might be affected due to the significant molecular weight enrichment. Some manipulations (integration of [                                     ]
might be required. Such post-synthetic reconstructions/additions will be readily carried out once a desired complex architectures
are obtained and tested for solubility.

 

Manpower: 2 Postdoc

 

Projected duration: [              ]

 

	I - Synthesis of CBD [         ]
    hybrid

 

 

	II - Synthesis of CBD [                ]
    hybrid

 

Two types of coupling strategies will
be applied: C-O bond formation (Pd or Cu catalysts will be used), and C-C bond formation, where [                  ]
molecule will undergo Heck cross-coupling reaction with CBD under Pd-Base conditions.

 

    	10

     

    

 

 

	III - Synthesis of CBD [                ]
    hybrid

 

Structural modifications of [                 ]
will be performed (as shown below) prior to it’s fusion with CBD

 

 

    	11

     

    

 

 

	IV - Synthesis of CBD [       ]
    hybrid

 

 

	Budget

 

Request for 50% upon signing and additional half way 50% after
6 months.

 

 

    	12

     

    

 

Appendix B

 

		1.	Royalties: the Company shall pay Yissum the
following royalties:

 

With respect to sales of
Products by the Company/affiliates [       ]
royalties from Net Sales of Products by the Company or its Affiliates (as such terms shall be defined in the License Agreement)
(“Company Royalties”), for a period ending with the earlier of (i) [         ]
from the First Commercial Sale or (ii) the expiration of any Yissum patent licensed to the Company for such product.

 

		b.	With respect
                                         to sales of Products by any Sublicensee: royalties at a rate equal to the lesser
                                         of (i) [                                ]
                                         of the Net Sales of Products by the particular Sublicensee (or its affiliates); or (ii)
                                         [                     ]
                                         of any proceeds, or consideration or benefit of any kind whatsoever, that the Company
                                         or its affiliates receive from such Sublicensee as a result of any sales of Products
                                         by the Sublicensee (or its Affiliates), provided, that such proceeds are not related
                                         to funding research and development costs of the Company.

 

		2.	Sublicense
                                         fee: [        ]
                                         on all consideration (other than royalties under Section 1) received by the Company or
                                         an affiliate as a result of the grant of a Sublicense, or an option to Sublicense (such
                                         as upfront payments, milestones payments), provided, such consideration shall not include
                                         payment to fund research and development costs of the Company.

 

		3.	Milestone payments:

 

		·	Upon
                                         commencement of the first in-human trial: [              ]

		·	Upon
                                         the commencement of a pivotal Phase IIb/Phase III trial: [              ]

		·	Upon
                                         Approval of an NDA in the US: [              ]

		·	Upon
                                         approval of an equivalent marketing application in any EU country: [              ]

		·	Upon
                                         the first approval of an equivalent marketing application in either China or Canada: [              ]

 

		4.	Territory: Worldwide unless Company determines not
to fund patent costs in a country which another company desires to fund, in which event such latter company shall have a right
to commercialize in that country; provided, that the Company has not previously paid royalties to Yissum based upon sales in that
country.

 

    	13Exhibit 10.4

 

	 	REDACTED
	 	*Certain identified
                                                        information has been excluded from

the exhibit because it is
both (i) not material and (ii)

would be competitively harmful
if publicly disclosed.*

 

		DEPARTMENT OF HEALTH AND HUMAN SERVICES	
        National Institute On Alcohol Abuse And Alcoholism

        National Institutes of Health

        5625 Fishers Lane

        Bethesda, MD 20892 USA

 

Second
Amendment

To
the Cooperative Research and Development Agreement

Between

The
National Institute on Alcohol Abuse and Alcoholism

And

Vital
Spark, Inc.

 

This Second Amendment (“Amendment
No. 2”) between the National Institute on Alcohol Abuse and Alcoholism (“IC”), which is a component
of the National Institutes of Health, an agency of the U.S. Department of Health and Human Services, having offices located at
5625 Fishers Lane, Bethesda, MD 20892, and Vital Spark, Inc. (“Collaborator”), having a principal
place of business at 420 Lexington Avenue, Suite 300, New York, New York 10170, and incorporated in the State of Delaware
(collectively, the “Parties”), will be effective as of the date of the last Authorized signature below (the
 “Amendment No. 2 Effective Date”).

 

WHEREAS, the Parties hereto entered
into a Cooperative Research and Development Agreement, with an Effective Date of January 11, 2018 and an Expiration Date
of January 11, 2020 (the “Agreement”), and subsequently executed a first amendment to the Agreement (“Amendment
No. 1”), with an effective date of October 31, 2018 (the “Amendment No. 1 Effective Date”).

 

WHEREAS, the Parties desire to modify
the Agreement; and,

 

WHEREAS, the purpose of this Amendment
No. 2 is to amend and modify the Agreement; and,

 

WHEREAS, pursuant to Amendment No.
1. the Parties agreed to defer the second-year funding of the Agreement, until the results of certain additional testing undertaken
by the IC were obtained; and,

 

WHEREAS, as a result of findings
of the aforementioned additional testing obtained by IC, the Collaborator has determined to proceed with the second year of the
Agreement; and,

 

WHEREAS, as a result of the aforementioned
additional testing, the Parties desire to modify the research plan described in Appendix A (hereafter referred to as the “Research
Plan”) of the Agreement; and,

 

WHEREAS, as a result of the modification
of the Research Plan, the Collaborator has agreed to increase the funding for the second year of the Agreement from one-hundred
thousand (USD $100,000.00) dollars to one hundred-eleven thousand, seven-hundred and forty (USD $111,740.00) dollars.

 

THEREFORE, the Parties hereby agree
to amend and modify the Agreement as follows:

 

	1)	The Parties agree to modify the Research Plan. Accordingly,
Appendix A of the Agreement is hereby amended to read as follows:

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 1 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

APPENDIX A

 

RESEARCH PLAN:

 

Introduction: Scleroderma
or systemic sclerosis (SSc) is an autoimmune, multi-organ connective tissue disease characterized by vascular dysfunction and
increased fibroblast activity resulting in fibrosis of the skin, heart, lungs, and ultimately internal organ failure leading
to death (1), with an estimated prevalence of SSc in the United States to be around 240 cases per 1 million adults (2). SSc
is a complex, heterogeneous disease with clinical forms ranging from limited skin involvement (limited cutaneous systemic
sclerosis) to forms with diffuse skin sclerosis and severe and often progressive internal organ involvement (diffuse
cutaneous SSc (3)). Pulmonary fibrosis and interstitial lung diseases (ILD) occur in about 60% of patients contributing to
mortality (4), while dermal fibrosis causes significant morbidity in scleroderma (5, 6). The etiology of SSc is unknown and
disease manifestations may vary from patient to patient. Environmental influences may act as risk factors for the development
of SSc (7, 8). Currently available single target therapies have not been effective either in mitigating the development of
SSc or inducing its regression. In view of the complex, multifactorial pathogenesis of SSc, its effective treatment may
require targeting multiple signaling pathways (9). Polypharmacology involves the design and use of pharmaceutical agents that
act on multiple targets or disease pathways (10), which is particularly desirable in the case of complex, multifactorial
diseases (11). Furthermore, the concept of “one drug – multiple targets” would minimize many unfavorable
features of combination treatments such as simpler pharmacokinetics, improved target organ exposure, and fewer drug-drug
interactions and adverse effects. This approach requires a systematic integration of different disciplines,
including synthetic chemistry, in vitro/in vivo pharmacological and preclinical testing, and clinical studies for
smoother translation from bench to bedside. SSc is one such disease that may benefit from the application of polypharmacology
(9).

 

This proposal seeks to explore two potential
therapeutic targets involved in pro-fibrogenic pathways, using a single molecular entity designed and developed ‘in-house’.
One of the targets is iNOS, an enzyme encoded by the NOS2 gene and responsible for generating pro-inflammatory, reactive
nitrogen species (12). The relevance of iNOS as a target is based on evidence for overproduction of nitric oxide (NO) in the pathogenesis
of SSc (13, 14). iNOS is expressed in the endothelium, smooth muscle cells, fibroblasts, macrophages and many other cell types,
is robustly induced by inflammatory mediators and cytokines (12), and its activity has been reported to increase in SSc (13). In
contrast, the activity of a constitutively expressed form of NOS located in the vascular endothelium (eNOS, encoded by the NOS3
gene) has been reported to be reduced in SSc (15), resulting in a vasoconstricted and proinflammatory environment in association
with tissue damage (16). At inflammatory sites, the iNOS-mediated formation of NO is increased in inflammatory cells such as macrophages
or activated fibroblasts. Immuno-histological studies of scleroderma skin show that, as the disease progresses to the later fibrotic
stages, the expression of iNOS is upregulated (17). Previous studies also demonstrate that SSc lung macrophages express high levels
of iNOS and produce a high quantity of ONOO’ anions (17). In SSc patients, increased production of NO is suggested by increased
expression of iNOS in endothelial cells, fibroblasts, mononuclear cells infiltrating SSc skin (16) and alveolar macrophages (15).
The pathogenic role of iNOS is eloquently dissected by the work of Cotton et al. which proposes the active role of iNOS-induced
NO production in endothelial cell damage and advances the concept of iNOS inhibition as a viable therapeutic strategy for SSc (18).
However, iNOS inhibitors used in preclinical studies lack oral bioavailability (19), whereas more recently developed, orally bioavailable
iNOS inhibitors had disappointingly low therapeutic efficacy in clinical trials involving inflammatory diseases (20).

 

An additional target that is becoming increasingly
relevant in the modulation of fibrotic responses is the endocannabinoid (EC) system. ECs are lipid-signaling molecules that act
through cannabinoid receptors CB1 and CB2. ECs acting via CB1R promote fibrosis in multiple organs including skin (21),
liver (22-24), kidney (25), and heart (26). Besides, CB1R activation is pro-inflammatory (27). CB1R have
recently been linked to radiation-induced pulmonary fibrosis in mice (28). Recent evidence including work in our lab indicate
that CB1R antagonism prevents fibroblast activation and exerts a potent antifibrotic effect (29). The role of CB1R
as a pro-fibrotic receptor has also been confirmed in fatty acid amide hydrolase knock-out mice, in which elevated levels of ECs
induced fibrosis in a CB1R-dependent manner (30). In addition to fibrosis, numerous studies have documented that an
overactive EC/CB1R system contributes to visceral obesity and its complications (31), including type-2 diabetes (27),
and also play a role in the pathology of alcoholic liver disease (32) and viral hepatitis (33). Conversely, CB1R blockade
has beneficial effects in preclinical models of these conditions as well as in overweight individuals with metabolic syndrome (34).
However, rimonabant and related brain-penetrant CB1R antagonists cause psychiatric side effects due to blockade of CB1R
in the CNS, which halted their therapeutic development. Non-brain-penetrant CB1R antagonists have recently been reported
to retain the metabolic benefit of globally acting compounds without blocking CB1R in the CNS and thus without related
behavioral effects (27, 35-37). Efforts to engage CB1Rs for mitigating fibrosis would require antagonists with limited
brain exposure in order to avoid neuropsychiatric side effects (37).

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 2 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

With these principles in mind, IC has developed
and patented orally bioavailable, dual-target compounds that selectively block peripheral CB1R due to their limited brain
penetrance and also directly inhibit iNOS activity (38). These compounds have several features for optimal therapeutic efficacy
and safety. The hybrid compound serves as a pro-drug and a carrier for the iNOS inhibitory moiety, facilitating its delivery to
target organs such as skin, kidney, lung, and liver, resulting in high target exposure. IC has identified lead compounds and screened
them for optimally druggable pharmacodynamic and pharmacokinetic properties. For the lead compound MRI-1867, CB1R was
the only high-affinity (Ki <1 μM) target among selected receptors, ion channels and enzymes (Cerep Safety44 screen, DiscoveRx
panel of 192 GPCRs) and had an acceptable safety and stability profile using non-GLP in vitro tests (AMES test, hERG assay,
microsomal stability, plasma stability, CYP inhibition, CYP phenotyping) (24). A proof of concept study in 2 mouse models of liver
fibrosis (24) and in bleomycin-induced lung fibrosis indicated improved anti-fibrotic efficacy relative to the efficacy of a single
target CB1R antagonist or iNOS inhibitor (39). The IC in vitro and in vivo data in murine models of liver
fibrosis and pulmonary fibrosis provide a strong rationale for testing this compound in dermal fibrosis models of scleroderma.

 

The scope of the CRADA Research Plan is
limited to the assessment of the therapeutic potential of CB1R/iNOS dual-target inhibitors in animal models of scleroderma
for the treatment and prevention of fibrotic conditions related to the progression of scleroderma.

 

Research Strategy:
The CRADA Parties will build upon the hypothesis that the EC/CB1R system and iNOS are both pro-fibrogenic, and
combined inhibition of these targets by a single compound would improve therapeutic outcome in scleroderma. Parties plan to test
the novel dual-target compound MRI-1867 in bleomycin-induced subcutaneous fibrosis model in multi drug resistance 1a and 1b [            ]/
breast cancer resistance protein [                                   .]

 

Bleomycin-induced scleroderma
model Subcutaneous injections of bleomycin induce skin and pulmonary fibrosis (40), quantifiable histologically and biochemically.
A recent modification in this protocol generated reproducible and more homogenous skin and lung fibrosis lesions mimicking human
SSc, with interstitial lung disease-like manifestations (41). However, IC investigators observed that daily subcutaneous
bleomycin administration significantly increased efflux transporters such as [          ,]
[          ] and [       ]
in skin that resulted in drastically reduced skin exposure to test compount (MRI-1867), which is a substrate for these transporters.
Therefore, this experimental artifact would preclude preclinical efficacy testing using wild-type mice in bleomycin-induced skin
fibrosis model. The IC investigators found that bleomycin also induced skin fibrosis in [                     ]
[                     ]
which was comparable to that in wt mice. Importantly, MRI-1867 skin exposure was not reduced in the [                 ]
and was similar to that in bleo-treated wildtype mice. Therefore [                                   ]
[       ] will be used in these proposed studies.

 

Specific Aim 1:

 

Previously conducted study will
be repeated testing S-MRI-1867 at [             ]
dose in [                                                                 ]
fibrosis model.

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 3 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

Approaches for Aim 1:

 

		1.1.	Skin abnormalities and fibrosis will be assessed histologically (H&E and Masson’s trichrome),
biochemically (hydroxyproline content) and by measuring profibrotic gene expression (TGFβ, αSMA, fibronectin, collagen, TIMP1).

 

Specific Aim 2: Dose ranging of
S-MRI-1867 for skin exposure

 

Approaches for Aim 2:

 

		2.1.	Tissue distribution and pharmacokinetics
                                         of S-MRI1867 will be tested in [                                    ]
                                         at different doses prior to starting dose ranging study in order to verify proportional
                                         exposure at different doses via single acute administration of the compound [                                    .]

 

Specific Aim 3: Assessing
effective dose range of S-MRI-1867 treatment in bleomycin-induced skin fibrosis in [                                        .]

 

Approaches for Aim 3:

 

S-MRI-1867 at doses of [                    ]
(maybe increase to [           ]
based on AIM1) will be used in treatment paradigm using 12 mice in each group. In the same study we will also include [           ]
of ibipinabant as a brain penetrant CB1R antagonist, which is also structural analogue of S-MRI-1867. Comparing ibipinabant
and S-MRI-1867 will help us understand the contribution of the secondary target to therapeutic efficacy.

 

		3.1.	Skin abnormalities and fibrosis will be assessed histologically (H&E and Masson’s trichrome)
and biochemically (hydroxy-proline content).

 

		3.2.	Protein and gene expression levels of CB1R and iNOS will be investigated by immunohistochemistry
and real-time PCR.

 

		3.3.	Endocannabinoids will be measured by LC-MS/MS.

 

		3.4.	Inflammatory and fibrogenic gene markers will be measured in a separate study using skin samples
after the dose assessment study has been completed.

 

Impact: Systemic sclerosis
is a debilitating, multifactorial, autoimmune condition, in which the body’s immune system attacks healthy tissues. While
certain mutations in human leukocyte antigen (HLA) genes have been implicated, numerous environmental factors have been associated
with altered progression of scleroderma. The CRADA Parties propose here an investigation into the potential therapeutic utility
of directly targeting CB1R and iNOS, with high translation potential, to treat and prevent fibrotic conditions related
to the progression of scleroderma. The goals for this project are to test the hypothesis that an overactivity of iNOS and CB1R
contribute to fibrogenesis in scleroderma, by analogy to our earlier findings with other forms of fibrosis. Parties propose to
explore the therapeutic efficacy of combined blockade of peripheral CB1R and iNOS in bleomycin-induced skin fibrosis
and inflammation and determine whether it offers therapeutic benefit over targeting only one of these proteins. In addition to
testing the NIAAA lead hybrid inhibitor, the Parties will test/develop additional molecular entities with druggable pharmacological
properties within this paradigm. The results of the proposed experiments will shed further light on the signaling pathways involved
in scleroderma and may uncover novel targets for its treatment and prevention.

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 4 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

Future Intentions:

 

Should both the results of
the CRADA Research Plan and the results from future IND-enabling studies warrant advancement of compound MRI-1867 into
clinical development for systemic sclerosis (scleroderma), it is the intent of the IC, after receiving approval from the
National Center for Advancing Translational Sciences (NCATS), to provide the CRADA Collaborator with either a cross-reference
letter of its Investigational New Drug Application for compound MRI-1867 to the U.S. Food and Drug Administration (FDA), or
access to the IND-enabling data (obtained through IC’s partnership with the NCATS Therapeutics for Rare and Neglected
Disease (TRND) program) for CRADA Collaborator to file a Collaborator-sponsored IND for compound MRI-1867 (or potentially
other CB1/iNOS dual action inhibitors identified pursuant to the performance of the CRADA Research Plan) in system sclerosis
(scleroderma). For clarity, these IND-enabling data will be used by the Collaborator solely to obtain an IND for the clinical
testing of the lead compound, MRI-1867 (or other CB1/iNOS dual action inhibitors identified pursuant to the performance of
the CRADA Research Plan), in systemic sclerosis, and will not be shared with any outside parties without the written consent
of the IC.

 

Personnel:

 

Malliga Iyer, Ph.D., is a synthetic
chemist with broad training and expertise in medicinal chemistry and analytical chemistry, which has enabled her to create a diverse
set of compounds for pharmacological testing. She has been responsible for the design, chemical synthesis and quality control of
novel dual-target compounds.

 

Resat Cinar, Pharm.D., Ph.D., is
a pharmacologist, with expertise in both in vitro and in vivo pharmacology and drug discovery. He has broad experience
in pharmacodynamics and pharmacokinetics, which has been indispensable for lead optimization of candidate drug molecules and efficacy
testing in animal models.

 

George Kunos, M.D., Ph.D., is head
of Laboratory and Scientific Director at NIAAA/ NIH. He trained many PhD students and post-doctoral fellows. He is a world-renowned
expert on the biology and pharmacology of the endocannabinoid system. Dr Kunos’ lab at NIH has characterized the pharmacological
profile and mechanism of metabolic action of potent, peripherally restricted CB1R antagonists/inverse agonists in rodent models
of obesity and diabetes (27, 35, 36, 43). In the models studied, such compounds offer similar metabolic benefits as brain-penetrant
CB1R antagonists without causing behavioral effects attributed to blockade of CB1R in the CNS.

 

Morris Laster, M.D., trained at
SUNY Albany, SUNY Downstate Medical Center and Case Western Reserve University Hospital. He is a healthcare executive/entrepreneur
with over 25 years of experience in the biopharmaceutical industry.

 

REFERENCES

 

		1.	Katsumoto TR, et al. (2011) The pathogenesis of systemic sclerosis. Annual review of pathology
6:509-537.

 

		2.	Mayes MD (2003) Scleroderma epidemiology. Rheum Dis Clin North Am 29(2):239-254.

 

		3.	Moinzadeh P, et al. (2015) Disease progression in systemic sclerosis-overlap syndrome is
significantly different from limited and diffuse cutaneous systemic sclerosis. Ann Rheum Dis 74(4):730-737.

 

		4.	Steen VD & Medsger TA (2007) Changes in causes of death in systemic sclerosis, 1972-2002. Ann
Rheum Dis 66(7):940-944.

 

		5.	de-Sa-Earp AP et al. (2013) Dermal dendritic cell population and blood vessels are diminished in
the skin of systemic sclerosis patients: relationship with fibrosis degree and disease duration. Am J Dermatopathol 35(4):438-444.

 

		6.	Akter T (2014) Recent advances in understanding the pathogenesis of scleroderma-interstitial lung
disease. Curr Rheumatol Rep 16(4):411.

 

		7.	Nietert PJ, et al. (1998) Is occupational organic solvent exposure a risk factor for scleroderma?
Arthritis Rheum 41(6):1111-1118.

 

		8.	McCormic et al. (2010) Occupational silica exposure as a risk factor for scleroderma: a meta-analysis.
Int Arch Occup Environ Health 83(7) 763-769.

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 5 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

		9.	Denton CP (2015) Systemic sclerosis:
                                         from pathogenesis to targeted therapy. Clinical and experimental rheumatology
                                         33(4 Suppl 92):S3-7.

 

		10.	Reddy AS & Zhang S (2013)
                                         Polypharmacology: drug discovery for the future. Expert review of clinical pharmacology
                                         6(1):41-47.

 

		11.	Hopkins AL (2008) Network pharmacology:
                                         the next paradigm in drug discovery. Nat Chem Biol 4(11):682-690.

 

		12.	Aktan F (2004) iNOS-mediated nitric
                                         oxide production and its regulation. Life Sci 75(6):639-653.

 

		13.	Dooley A, et al. (2012) Modulation
                                         of fibrosis in systemic sclerosis by nitric oxide and antioxidants. Cardiol Res Pract
                                         2012:521958.

 

		14.	Sud A, Khullar M, Wanchu A, &
                                         Bambery P (2000) Increased nitric oxide production in patients with systemic sclerosis.
                                         Nitric Oxide 4(6):615-619.

 

		15.	Matucci Cerinic M et al(2002)
                                         Beauty and the beast. The nitric oxide paradox in systemic sclerosis. Rheumatology
                                         (Oxford) 41(8):843-847.

 

		16.	Yamamoto T et al. (1998) Nitric
                                         oxide production and inducible nitric oxide synthase expression in systemic sclerosis.
                                         J Rheumatol 25(2):314-317.

 

		17.	Failli P, et al. (2002)
                                         Effect of N-acetyl-L-cysteine on peroxynitrite and superoxide anion production of lung
                                         alveolar macrophages in systemic sclerosis. Nitric Oxide 7(4):277-282.

 

		18.	Cotton SA et al. (1999) Endothelial
                                         expression of nitric oxide synthases and nitrotyrosine in systemic sclerosis skin. J
                                         Pathol 189(2):273-278.

 

		19.	Lopez-Sanchez LM, et al. (2010)
                                         Inhibition of nitric oxide synthesis during induced cholestasis ameliorates hepatocellular
                                         injury by facilitating S-nitrosothiol homeostasis. Lab Invest 90(1):116-127.

 

		20.	Hellio le Graverand MP, et
                                         al. (2013) A 2-year randomised, double-blind, placebo-controlled, multicentre study
                                         of oral selective iNOS inhibitor, cindunistat (SD-6010), in patients with symptomatic
                                         osteoarthritis of the knee. Annals of the rheumatic diseases 72(2):187-195.

 

		21.	Lazzerini PE, et al. (2012)
                                         Adenosine A2A receptor activation stimulates collagen production in sclerodermic dermal
                                         fibroblasts either directly and through a cross-talk with the cannabinoid system. Journal
                                         of molecular medicine 90(3):331-342.

 

		22.	Teixeira-Clerc F, et al. (2006)
                                         CB1 cannabinoid receptor antagonism: a new strategy for the treatment of liver fibrosis.
                                         Nat Med 12(6):671-676.

 

		23.	Patsenker E, et al. (2011)
                                         Cannabinoid receptor type I modulates alcohol-induced liver fibrosis. Mol Med 17(11-12):1285-1294.

 

		24.	Cinar R, et al. Hybrid
                                         inhibitor of peripheral cannabinoid 1 receptors and inducible nitric oxide synthase mitigates
                                         of liver fibrosis. Journal of Clinical Investigation Insight, In press, 2016.

 

		25.	Lin CL, et al. (2014) Cannabinoid
                                         receptor 1 disturbance of PPARgamma2 augments hyperglycemia induction of mesangial inflammation
                                         and fibrosis in renal glomeruli. Journal of molecular medicine 92(7):779-792.

 

		26.	Slavic S, et al. (2013)
                                         Cannabinoid receptor 1 inhibition improves cardiac function and remodelling after myocardial
                                         infarction and in experimental metabolic syndrome. Journal of molecular medicine
                                         91(7):811-823.

 

		27.	Jourdan T, et al. (2013)
                                         Activation of the Nlrp3 inflammasome in infiltrating macrophages by endocannabinoids
                                         mediates beta cell loss in type 2 diabetes. Nat Med 19(9):1132-1140.

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 6 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

		28.	Bronova I, et al. (2015) Peripheral targeting of CB1 cannabinoid receptors protects from
radiation-induced pulmonary fibrosis. American Journal of Respiratory Cell and Molecular Biology.

 

		29.	Marquart S, et al. (2010) Inactivation of the cannabinoid receptor CB1 prevents leukocyte
infiltration and experimental fibrosis. Arthritis Rheum 62(11):3467-3476.

 

		30.	Palumbo-Zerr K, et al. (2012) Inactivation of fatty acid amide hydrolase exacerbates experimental
fibrosis by enhanced endocannabinoid-mediated activation of CB1. Ann Rheum Dis 71(12):2051-2054.

 

		31.	Silvestri C et al. (2013) The endocannabinoid system in energy homeostasis and the etiopathology
of metabolic disorders. Cell Metab 17(4):475-490.

 

		32.	Jeong WI, et al. (2008) Paracrine activation of hepatic CB1 receptors by stellate cell-derived endocannabinoids mediates alcoholic fatty liver. Cell Metab 7(3):227-235.

 

		33.	Hezode C, et al. (2005) Daily cannabis smoking as a risk factor for progression of fibrosis
in chronic hepatitis C. Hepatology 42(1) 63-71.

 

		34.	Despres JP et al.(2005) Effects of rimonabant on metabolic risk factors in overweight patients
with dyslipidemia. N Engl J Med 353(20):2121-2134.

 

		35.	Tam J, et al. (2012) Peripheral cannabinoid-1 receptor inverse agonism reduces obesity by
reversing leptin resistance. Cell Metab 16(2):167-179.

 

		36.	Cinar R, et al. (2014) Hepatic cannabinoid-1 receptors mediate diet-induced insulin resistance
by increasing de novo synthesis of long-chain ceramides. Hepatology 59(1):143-153.

 

		37.	Tam J, et al. (2010) Peripheral CB1 cannabinoid receptor blockade improves cardiometabolic
risk in mouse models of obesity. J Clin Invest 120(8):2953-2966.

 

		38.	Kunos G, Iyer MR, Cinar R, & Rice KC (2014) WO 2014/078309 A1.

 

		39	Cinar R et al. Dual-targeting on peripheral CB1R and iNOS for inhibition provides effective
anti-fibrotic therapy in IPF. In preparation

 

		40.	Tsujino K & Sheppard D (2016) Critical Appraisal of the Utility and Limitations of Animal Models
of Scleroderma. Curr Rheumatol Rep 18(1):4.

 

		41.	Liang M. et al. (2015) A modified murine model of systemic sclerosis: bleomycin given
                                                                by pump infusion induced skin and pulmonary inflammation and fibrosis. Lab Invest 95(3):342-350.

 

		42.	Morin F, Kavian N, & Batteux F (2015) Animal models of systemic sclerosis. Curr Pharm Des
21(18):2365-2379.

 

		43.	Jourdan T, et al. (2014) Overactive cannabinoid 1 receptor in podocytes drives type 2 diabetic
nephropathy. Proc Natl Acad Sci U S A.

 

		2)	The Parties agree to modify Appendix B to modify the funding contribution of the Collaborator
to the Agreement. Accordingly, the “Funding Contribution” disclosed in Appendix B of the Agreement is hereby amended
to read as follows:

 

Funding Contribution

 

Collaborator agrees to provide
funds in the amount of one hundred-eleven thousand, seven hundred and forty (USD $111,740.00) dollars for year two of the
CRADA, for the IC to use to acquire technical, statistical, and administrative support for the research activities, as well as
to pay for supplies and travel expenses.

 

Collaborator will provide the
funds indicated in paragraph above, in two equal payments of fifty-five thousand, eight hundred and seventy (USD $55,870.00)
dollars each. The first payment will be provided to the IC within three (3) business days of the Amendment No. 2
Effective Date, and the second payment will be provided to the IC within six (6) months of the Amendment No. 2 Effective Date.

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 7 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

As of the Amendment No. 2
Effective Date, Collaborator has paid the amount of one-hundred-thirty thousand (USD $130,000.00) dollars for year one of the
CRADA. For the term of the CRADA, the total funds to be provided by Collaborator will be two hundred-forty-one thousand, seven-hundred
and forty (USD $241,740.00) dollars.

 

The Collaborator agrees that
the IC can allocate the funding between the various categories in support of the CRADA research as the IC sees fit.

 

CRADA Payments:

 

Collaborator will make checks
payable to the National Institute on Alcohol Abuse and Alcoholism, will reference the CRADA number and title on each check, and
will send them via trackable mail or courier to:

 

Judit O’Connor

National Institute on Alcohol
Abuse and Alcoholism

5635 Fishers Lane, Room 3011

Bethesda, MD 20892-9304

 

CRADA Travel Payments:

 

Travel arrangements for all
Government staff will be made in accordance with the Federal Travel Rules and Regulations, whether arranged by IC and funded using
either appropriated funds or CRADA funds, or arranged and funded directly by Collaborator.

 

	3)	Except as amended herein, all of the terms and conditions of the Agreement and Amendment No.
1 will remain in full force and effect, and all defined terms of the Agreement and Amendment No. 1 will have the same meaning in
this Amendment No. 2, as defined in those instruments.

 

	4)	This Amendment No. 2 shall be construed in accordance with the laws of the United States, as
interpreted and applied by the Federal courts in the District of Columbia.

 

	5)	This Amendment No. 2 may be executed in counterparts, each of which shall be deemed an original,
and all of which, taken together, shall constitute one and the same instrument. A facsimile, scanned electronic signature, or certified
electronic signature shall be as effective as an original signature.

 

SIGNATURES BEGIN ON THE NEXT PAGE

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 8 of 9

    	 	
	 	National Institute
 on Alcohol Abuse

and Alcoholism

    

 

	For
    the National Institute On Alcohol Abuse And Alcoholism

 

	Signed
    by:	/s/ George F. Koob	 
	 	George F. Koob, Ph.D.	 
	 	Director,	 
	 	National Institute on Alcohol Abuse and Alcoholism (NIAAA)	 
	 	 	 
	Date:	5-6-19	 

 

Mailing Address for Notices:

 

National Institute on Alcohol Abuse and
Alcoholism (NIAAA)

Attn: Technology Development Coordinator

National Institutes of Health

5635 Fishers Lane Room 2038

Bethesda, MD 20892

 

	For Vital Spark, Inc.

 

	Signed by:	/s/ Morris
    Laster, MD	 
	 	Morris Laster, M.D.	 
	 	Chief Executive Officer	 
	 	Vital Spark, Inc.	 
	 	 	 
	Date:	May 6, 2019	 

 

Mailing Address for Notices:

 

Vital Spark, Inc.

420 Lexington Avenue, Suite 300

New York, New York 10170

 

    	NIAAA-Vital Spark, Inc. Standard CRADA	 
	Amendment No. 2	Page 9 of 9

Source: [{"source": "alea-institute/alea-institute/kl3m-data-edgar-agreements/train-00297-of-00352.parquet"}, [{"source": "alea-institute/alea-institute/kl3m-data-edgar-agreements/train-00297-of-00352.parquet"}]]