UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 10-K

☒ ANNUAL REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934

For the fiscal year ended December 31, 2025

☐ TRANSITION REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934

For the transition period from ___ to ___

Commission file number 001-41596

CADRENAL THERAPEUTICS, INC.

(Exact name of registrant as specified in its charter)

Delaware		88-0860746
(State or other jurisdiction of incorporation or organization)		(I.R.S. Employer Identification No.)

822 A1A North, Suite 306 Ponte Vedra, Florida		32082
(Address of principal executive offices)		(Zip Code)

Registrant’s telephone number, including area code: (904) 300-0701

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

Title of each class		Trading Symbol(s)		Name of each exchange on which registered
Common Stock, par value $0.001 per share		CVKD		The Nasdaq Stock Market, LLC (The Nasdaq Capital Market)

Securities registered pursuant to Section 12(g) of the Act: None

Indicate by check mark if the registrant is a well-known seasoned issuer, as defined in Rule 405 of the Securities Act. Yes ☐ No ☒

Indicate by check mark if the registrant is not required to file reports pursuant to Section 13 or Section 15(d) of the Act. Yes ☐ No ☒

Indicate by check mark whether the registrant (1) has filed all reports required to be filed by Section 13 or 15(d) of the Securities Exchange Act of 1934 during the preceding 12 months (or for such shorter period that the registrant was required to file such reports), and (2) has been subject to such filing requirements for the past 90 days.

Yes ☒ No ☐

Indicate by check mark whether the registrant has submitted electronically every Interactive Data File required to be submitted pursuant to Rule 405 of Regulation S-T (§232.405 of this chapter) during the preceding 12 months (or for such shorter period that the registrant was required to submit such files).

Yes ☒ No ☐

Indicate by check mark whether the registrant is a large accelerated filer, an accelerated filer, a non-accelerated filer, a smaller reporting company or an emerging growth company. See the definitions of “large accelerated filer,” “accelerated filer”, “smaller reporting company” and “emerging growth company” in Rule 12b-2 of the Exchange Act:

Large accelerated filer	☐	Accelerated filer	☐
Non-accelerated filer	☒	Smaller reporting company	☒
		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. ☐

Indicate by check mark whether the registrant has filed a report on and attestation to its management’s assessment of the effectiveness of its internal control over financial reporting under Section 404(b) of the Sarbanes-Oxley Act (15 U.S.C. 7262(b)) by the registered public accounting firm that prepared or issued its audit report. ☐

If securities are registered pursuant to Section 12(b) of the Act, indicate by check mark whether the financial statements of the registrant included in the filing reflect the correction of an error to previously issued financial statements. ☐

Indicate by check mark whether any of those error corrections are restatements that required a recovery analysis of incentive- based compensation received by any of the registrant’s executive officers during the relevant recovery period pursuant to §240.10D-1(b). ☐

Indicate by check mark whether the registrant is a shell company (as defined in Rule 12b-2 of the Exchange Act). Yes ☐ No ☒

The aggregate market value of the voting and non-voting common equity held by non-affiliates of the registrant, based on the closing price of $12.05 per share of the registrant’s common stock on June 30, 2025, as reported by the Nasdaq Capital Market on such date, was approximately $24,868,103.

As of March 27, 2026, there were 2,506,817 shares of Common Stock, $0.001 par value per share, outstanding.

DOCUMENTS INCORPORATED BY REFERENCE: None

CADRENAL THERAPEUTICS, INC.

		Page
PART I		1

Item 1.	Business	3
Item 1A.	Risk Factors	25
Item 1B.	Unresolved Staff Comments	63
Item 1C.	Cybersecurity	63
Item 2.	Properties	63
Item 3.	Legal Proceedings	63
Item 4.	Mine Safety Disclosures	63

PART II		64

Item 5.	Market for Registrant’s Common Equity, Related Stockholder Matters and Issuer Purchases of Equity Securities	64
Item 6.	[Reserved]	65
Item 7.	Management’s Discussion and Analysis of Financial Condition and Results of Operations	65
Item 7A.	Quantitative and Qualitative Disclosures About Market Risk	67
Item 8.	Financial Statements and Supplementary Data	F-1
Item 9.	Changes in and Disagreements With Accountants on Accounting and Financial Disclosure	68
Item 9A.	Controls and Procedures	68
Item 9B.	Other Information	69
Item 9C.	Disclosure Regarding Foreign Jurisdictions that Prevent Inspections	69

PART III		70

Item 10.	Directors, Executive Officers and Corporate Governance	70
Item 11.	Executive Compensation	77
Item 12.	Security Ownership of Certain Beneficial Owners and Management and Related Stockholder Matters	84
Item 13.	Certain Relationships and Related Transactions, and Director Independence	86
Item 14.	Principal Accountant Fees and Services	87

PART IV		88

Item 15.	Exhibits and Financial Statement Schedules	88
Item 16.	Form 10-K Summary	88

PART I

Forward-Looking Statements

This Annual Report on Form 10-K (this “Annual Report”) contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended (the “Securities Act”), and Section 21E of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), that involve substantial risks and uncertainties. The forward-looking statements are contained principally in Part I, Item 1. “Business,” Part I, Item 1A. “Risk Factors,” and Part II, Item 7. “Management’s Discussion and Analysis of Financial Condition and Results of Operations,” but are also contained elsewhere in this Annual Report in some cases you can identify forward-looking statements by terminology such as “may,” “should,” “potential,” “continue,” “expects,” “anticipates,” “intends,” “plans,” “believes,” “estimates,” and similar expressions. These statements are based on our current beliefs, expectations, and assumptions and are subject to a number of risks and uncertainties, many of which are difficult to predict and generally beyond our control, that could cause actual results to differ materially from those expressed, projected or implied in or by the forward-looking statements.

You should refer to Part I, Item 1A. “Risk Factors” section of this Annual Report for a discussion of important factors that may cause our actual results to differ materially from those expressed or implied by our forward-looking statements. As a result of these factors, we cannot assure you that the forward-looking statements in this Annual Report will prove to be accurate. Furthermore, if our forward-looking statements prove to be inaccurate, the inaccuracy may be material. In light of the significant uncertainties in these forward-looking statements, you should not regard these statements as a representation or warranty by us or any other person that we will achieve our objectives and plans in any specified time frame, or at all. We do not undertake any obligation to update any forward-looking statements. Unless the context requires otherwise, references to “we,” “us,” “our,” and “Cadrenal,” refer to Cadrenal Therapeutics, Inc.

This Annual Report also contains market data related to our business and industry. These market data include projections that are based on a number of assumptions. If these assumptions turn out to be incorrect, actual results may differ from the projections based on these assumptions. As a result, our markets may not grow at the rates projected by these data, or at all. The failure of these markets to grow at these projected rates may harm on our business, results of operations, financial condition and the market price of our common stock, par value $0.001 per share (the “Common Stock”).

Summary Risk Factors

Our business faces significant risks and uncertainties of which investors should be aware before making a decision to invest in our Common Stock. If any of the following risks are realized, our business, financial condition and results of operations could be materially and adversely affected. The following is a summary of the more significant risks relating to the Company. A more detailed description of our risk factors is set forth below under the caption “Risk Factors” in Item 1A in Part I of this Annual Report.

Risks Related to Our Financial Position and Need for Capital

	●	Our financial statements have been prepared assuming that we will continue as a going concern.
	●	Any shutdown of the U.S. federal government may adversely affect our business.
	●	We are a clinical development biopharmaceutical company with a limited operating history.
	●	We have a limited operating history upon which to evaluate our ability to commercialize our product candidate.
	●	We have a limited operating history, a history of losses and expect to continue to incur losses.
	●	We may never become profitable or, if achieved, be able to sustain profitability.

	●	Our cash and the proceeds from our financings will only fund our operations for a limited time.
	●	We will need to raise additional capital.
	●	Our need for future financing may result in the issuance of additional securities, which will cause investors to experience dilution.

Risks Related to Product Development, Regulatory Approval, Manufacturing and Commercialization

	●	Our future success depends heavily on review of our Phase 3 trial protocol by the U.S. Food and Drug Administration (the “FDA”) and commencement of our Phase 3 clinical trial.
	●	The 12-LOX platform of assets is subject to significant clinical risks that could impede our ability to advance CAD-1005 or our second-generation oral candidates.
	●	Inadequate funding for the FDA, the SEC and other government agencies, including from government shutdowns, or other disruptions to these agencies’ staffing and operations could negatively impact our business.
	●	Our business is dependent upon the success of our product candidates, each of which require additional clinical testing.
	●	Our business is substantially dependent on a license agreement, and the termination, non-renewal or failure to maintain that agreement could materially and adversely affect our business, financial condition and prospects.
	●	All of our current data for our product candidates are the results of clinical trials conducted by third parties.
	●	Our development efforts may not generate data sufficient to support regulatory approval and the FDA and/or the European Medicines Agency (the “EMA”) may require additional clinical testing.

	●	Even if we complete our clinical trials, we may not receive regulatory approval for any of our product candidates.
	●	Orphan drug designation does not translate to approval and, even if we obtain FDA approval, we may not enjoy marketing exclusivity or other expected benefits.
	●	Fast Track designation and Orphan Drug Designation does not assure FDA or any other regulatory approval.
	●	Even if we obtain regulatory approval, we may not enjoy marketing exclusivity and we may face other difficulties.
	●	Clinical trials are very expensive, time-consuming and difficult to design and implement.
	●	We may experience delays in the enrollment of patients in any or all of our clinical trials.
	●	If any of our product candidates are approved, our success depends on our commercialization efforts and market acceptance.

	●	Our product candidates may fail to achieve the degree of market acceptance by physicians, patients, healthcare payors and others in the medical community necessary for commercial success.
	●	We have never submitted a New Drug Application to the FDA or comparable applications to other regulatory authorities.

	●	Any product candidate if approved for commercialization will remain subject to regulatory obligations and other restrictions.
	●	After approval, our products could be subject to labeling and other restrictions and we may be required to withdraw from the market or be subject to penalties if we fail to comply with regulatory requirements.
	●	We are subject to federal and state obligations and regulations applicable to our marketing practices.
	●	We rely, or will rely, on third-party manufacturers to produce our product candidates.
	●	If the manufacturer fails to comply with stringent regulations, we may face delays.
	●	We face substantial competition.
	●	Serious adverse effects may be identified with respect to our products candidates, which may harm our business.
	●	Recently enacted and future legislation may affect marketing approval and commercialization of our product candidates.
	●	We may be subject to penalties if we violate healthcare fraud and abuse laws or price reporting laws.
	●	Our ability to generate product revenues will be diminished if our products sell for inadequate prices.
	●	The impact of recent healthcare reform legislation in healthcare spending could adversely effect our business.
	●	We will rely on third parties to conduct all of our clinical trials.
	●	We currently do not have any distribution, marketing, support or sales capabilities.
	●	Our employees, contractors, consultants, commercial partners and vendors may engage in misconduct.
	●	If we are not successful in establishing a sales force, our ability to generate sales and profits will be limited.
	●	We plan to rely on third parties to develop, commercialize, market and promote our products.
	●	Our future growth depends, in part, on our ability to penetrate foreign markets.
	●	Global health crises may adversely affect our planned operations.
	●	Compliance with regulations regarding the treatment of animals could increase our costs.

General Company-Related Risks

	●	Our business depends upon our ability to attract and keep senior management and key scientific personnel.
	●	We will need to increase the size of our organization, and we may experience difficulties managing this.
	●	If product liability lawsuits are brought against us, we may incur substantial liabilities.
	●	Computer system failures could be costly and expose us to litigation and government enforcement actions.
	●	We are increasingly dependent on information technology and our systems face certain risks.
	●	Any failure to maintain the security of information relating to our patients, customers, employees and suppliers, whether as a result of cybersecurity attacks or otherwise, could disrupt our operations and harm our reputation.
	●	Our use of artificial intelligence presents risks that could adversely affect our business.
	●	Acquisitions of other businesses could harm our operating results.
	●	Declining general economic or business conditions may have a negative impact on our business.

Risks Related to Our Intellectual Property

	●	We may be unable to obtain and maintain market exclusivity or patent protection for our product candidates.
	●	We may become involved in intellectual property lawsuits, which could be costly and time consuming.
	●	If we are sued for infringing the intellectual property rights of third parties, such litigation could be costly and time-consuming and could prevent or delay us from developing or commercializing our product candidates.
	●	Patent law changes in the United States and other jurisdictions could diminish the value of patents.
	●	Patent protection depends on compliance with requirements imposed by governmental patent agencies.
	●	We may not be able to enforce our intellectual property rights throughout the world.
	●	Our U.S. patents and foreign patents for tecarfarin have expired.
	●	We may be subject to claims by third parties asserting that our employees or we have misappropriated their intellectual property, or claiming ownership of what we regard as our own intellectual property.

Risks Related to Ownership of Our Common Stock

	●	An active public trading market for our Common Stock may not be maintained.
	●	We cannot be assured that we will be able to maintain our listing on the Nasdaq Capital Market.

	●	Our stock price has been extremely volatile.
	●	Even if our product candidates receive FDA approval, the trading price of our Common Stock may not increase, and may decline.
	●	If favorable research or reports about us are not published our stock price could decline.
	●	Our Chief Executive Officer can exercise significant control over our Company.
	●	Sales of Common Stock could result in dilution and depress the market price of our Common Stock.
	●	Our charter documents have anti-takeover provisions.
	●	Our amended and restated certificate of incorporation and amended and restated bylaws provide that the Court of Chancery of the State of Delaware or the federal district court for the District of Delaware is the exclusive forum for certain disputes between us and our stockholders.
	●	Claims for indemnification by our directors and officers may reduce our available funds.
	●	We do not intend to pay dividends in the foreseeable future.
	●	Certain members of our management team have limited experience managing a public company.
	●	We have incurred significant increased costs as a result of operating as a public company and expect to incur additional costs when we commence clinical trials.
	●	We are an emerging growth company and may avail ourselves of reduced disclosure requirements or extended transition periods for complying with new or revised accounting standards.
	●	There is no public market for our outstanding warrants.
	●	Holders of our outstanding warrants will have no rights as common stockholders with respect to the shares of our Common Stock underlying the warrants until such holders exercise their warrants and acquire our Common Stock, except as otherwise provided in the warrants.

Item 1. Business.

The Company

We are a late-stage biopharmaceutical company advancing novel therapies for life-threatening immune and thrombotic conditions. As a result of our acquisition of a 12-lipoxygenase (“12-LOX”) platform of assets in December 2025 (as described in more detail below), we transitioned our primary strategic focus to the development of CAD-1005 for the treatment of immune-mediated and thrombotic disorders. Our lead product candidate, CAD-1005, is a first-in-class selective 12-LOX inhibitor being developed to treat heparin-induced thrombocytopenia (“HIT”), a deadly immune-mediated thrombotic disorder. CAD-1005 has been evaluated in a blinded, placebo-controlled study Phase 2 clinical trial of 24 patients as well as Phase 1 clinical trials in more than 100 patients. On March 26, 2026, we completed our End-of-Phase 2 (“EOP2”) meeting with the FDA and clarified a potential registrational path for our planned Phase 3 pivotal trial of CAD-1005 in patients with HIT. Our Phase 3 trial protocol will still be subject to additional information which may be set forth in the final meeting minutes from the FDA and any further comments we may receive from the FDA upon their review of the protocol. CAD-1005 has an orphan drug designation (“ODD”) from the FDA for the prophylaxis of thrombosis in patients with HIT, as well as an FDA Fast Track designation for the treatment and prevention of HIT, and an orphan designation from the EMA for the treatment of platelet-activating factor 4 disorders.

Our broader pipeline includes two additional clinical-stage assets—tecarfarin and frunexian. Tecarfarin is an oral vitamin K antagonist (“VKA”) (a warfarin replacement for patients with complex needs) designed to prevent heart attacks, strokes, and deaths due to blood clots in patients requiring chronic anticoagulation. Specifically, our focus for tecarfarin is for chronic use in patients with kidney dysfunction or left ventricular assist devices (“LVADs”). Tecarfarin has been specifically designed to overcome metabolic factors that can make warfarin less reliable. Frunexian is a first-in-class, Phase 2-ready intravenous (“IV”) Factor XIa inhibitor designed for acute care settings where contact activation of coagulation by medical devices or artificial surfaces is significant. Frunexian is the only IV FXIa inhibitor in clinical development that targets the acute/critical care hospital setting exclusively.

Recent Developments

Veralox Asset Purchase

On December 10, 2025, we entered into an Asset Purchase Agreement (the “Veralox Purchase Agreement”) with Veralox Therapeutics Inc., a Delaware corporation (“Veralox”), pursuant to which Veralox sold to us all, or substantially all, of its right title and interest in assets owned or otherwise used or held for use by Veralox in connection with the compound known as CAD-1005 (formerly “VLX-1005”), and all back-up and follow-on compounds, including the CAD-2000 (formerly “VLX-2000”) series (the “Compounds”), including, without limitation, all intellectual property related to the Compounds, all inventory related to the Compounds, certain contracts including a license agreement, all Permits and other Governmental Authorizations and Books and Records (as such terms are defined in the Veralox Purchase Agreement), free and clear of any liens (the “Veralox Assets”). The transactions contemplated by the Veralox Purchase Agreement were consummated on December 10, 2025.

The Veralox Assets also include the assignment of an Amended and Restated Exclusive License Agreement by and between Veralox and Old Dominion University, as successor in interest to Eastern Virginia Medical School (“Licensor”), dated as of May 1, 2020, as amended on December 9, 2025 pursuant to a First Amendment to Amended and Restated Exclusive License Agreement (the “Amendment to License Agreement”) by and between Old Dominion University, as successor in interest to Eastern Virginia Medical School, and Veralox (as amended, collectively, the “Old Dominion License Agreement”), pursuant to which Licensor granted Veralox an exclusive worldwide license under the EVMS Patent Rights (as such term is defined in the Old Dominion License Agreement) related to the development and commercialization of 4-((2-Hydroxy-3-MethoxyBenzyl)Amino) Benzenesulfonamide Derivatives as 12-Lipoxygenase Inhibitors.

See “Veralox Purchase Agreement” and “Old Dominion License Agreement” below for more detailed descriptions of the Veralox Purchase Agreement and the Old Dominion License Agreement.

Our Strategy

Our overarching goal at Cadrenal is to advance novel therapies for life-threatening immune and thrombotic conditions. Our current primary focus is advancing a transformative therapeutic approach for the treatment of HIT. On March 26, 2026, we completed our EOP2 meeting with the FDA and clarified a potential registrational path for our planned Phase 3 pivotal trial of CAD-1005 in patients with HIT. Our Phase 3 trial protocol will still be subject to additional information which may be set forth in the final meeting minutes from the FDA and any further comments we may receive from the FDA upon their review of the protocol. Commencement of a pivotal Phase 3 clinical trial in patients with HIT will also be subject to obtaining sufficient financing.

If we are successful in obtaining FDA approval of CAD-1005 for our first indication, we intend to seek to expand the label for CAD-1005 through additional filings, to explore the full spectrum of applications where we believe CAD-1005 can improve on existing standard treatment; including diabetes, atherosclerosis and chronic vascular inflammation and hyper-inflammatory responses, as seen in severe respiratory infections.

CAD-1005

Our lead product candidate, CAD-1005, is a first-in-class selective 12-LOX inhibitor being developed for the treatment of HIT, a deadly immune-mediated thrombotic disorder. CAD-1005 is designed to selectively inhibit 12-LOX, a pathway integral to the primary immune mechanisms driving HIT. Unlike existing therapies for HIT, which are only directed at preventing thrombotic complications, this approach addresses the primary underlying pathophysiology of HIT. CAD-1005 has an ODD from the FDA for prophylaxis of thrombosis in patients with HIT, as well as an FDA Fast Track designation for the treatment and prevention of HIT, and an orphan designation from the EMA for the treatment of platelet-activating factor 4 disorders.

Heparin-Induced Thrombocytopenia (HIT)

Heparin is the most widely used parenteral anticoagulant in modern-day practice. HIT is a serious, life-threatening prothrombotic complication of heparin administration, with high morbidity and mortality. HIT arises as a consequence of an immune reaction to endogenous platelet factor 4 (PF4) bound to exogenous heparin. Binding of HIT antibodies to platelet FcγRIIa (the platelet IgG receptor) and the FcγRI receptor (CD64) on monocytes results in the generation of thrombin, tissue factor, platelet-fibrin thrombi, procoagulant microparticles, and further PF4 release, creating a vicious cycle of additional platelet activation and resulting in a high likelihood of adverse thrombotic events. Argatroban and bivalirudin, both non-heparin-directed thrombin inhibitors, were approved in the United States for the treatment of HIT in the early 2000s, but, as parenteral anticoagulants, they only limit the progression of thrombus and do not address the underlying immune-mediated, platelet-centric pathophysiology of the disease. Since their approval, no additional treatments have been approved to prevent or treat HIT. Moreover, despite the use of such parenteral non-heparin anticoagulants, severe thrombotic complications of HIT occur frequently. Recent findings reported by Shatzel et al. and Ramadan et al. highlight the high incidence and clinical burden of thrombotic complications in contemporary HIT patients, highlighting the limitations of existing therapies. Therefore, we are developing a new drug candidate designed to directly address the pathophysiology of HIT by targeting platelet 12-LOX and thereby interrupting a vicious cycle of immune-mediated platelet activation.

12-LOX Inhibition and CAD-1005

12-LOX is highly expressed in human platelets and catalyzes the formation of 12-hydroxyeicosatetraenoic acid (12-HETE), which is a key intermediary signaling molecule in FcγRIIa-mediated platelet activation. Growing scientific evidence has identified 12-LOX as a key mediator of platelet activation and immune thrombotic responses. Foundational work by McKenzie et al. (2022) significantly advanced the understanding of 12-LOX signaling in platelet-driven immune thrombosis, including in HIT, supporting the 12-LOX pathway as a compelling therapeutic target. Pharmacologic inhibition of 12-LOX has been shown to suppress platelet activation, while having minimal impact on normal hemostasis and without increasing bleeding risk, a common limitation of current antiplatelet therapies. Historically, however, industry-wide drug development efforts targeting 12-LOX have been hindered by a lack of selectivity, raising concerns about off-target effects and safety. This challenge has limited the development of earlier 12-LOX inhibitors by other developers, none of which advanced to clinical stage development.

CAD-1005 is a potent and selective inhibitor of 12-LOX and is the only such inhibitor currently in clinical-stage development. It represents a novel approach to reduce the risk of severe thrombotic events in patients with HIT by specifically targeting a key platelet inflammatory signaling pathway that is believed to play a major role in HIT. In animal models of HIT, CAD-1005 has been shown to prevent or treat HIT and halt the development of both thrombocytopenia and abnormal blood clots, and has not been associated with increased bleeding in either animals or healthy human volunteers. The 12-LOX portfolio obtained from Veralox includes both parenteral (injectable) and oral second-generation candidates, addressing a range of acute and chronic conditions.

Pre-Clinical Data

In vivo inhibition of 12-HETE synthesis and the efficacy of CAD-1005 have been demonstrated in animal models of thrombosis and in immune-mediated thrombocytopenia and thrombosis. Importantly, this impact on thrombosis was not accompanied by increases in bleeding. In mice expressing the human immune receptor on their platelets, Veralox showed that administration of CAD-1005 following HIT induction resulted in blunted thrombocytopenia and reduced platelet activation and thrombus formation. Veralox further demonstrated that coagulation (assessed by thromboelastography) was not impacted by CAD-1005, while the direct thrombin inhibitor argatroban significantly delayed the onset of coagulation and clot formation. Moreover, bleeding times in these mice were not altered by CAD-1005, whereas argatroban-treated mice required cauterization to stop bleeding. Finally, human whole blood, as measured by whole-blood aggregometry and high-shear arterial flow chamber experiments, was protected from platelet activation and clot formation in the presence of CAD-1005. Thus, preclinical studies demonstrate the potential effectiveness of CAD-1005 in blocking platelet activation, clot formation, and thrombosis in both mouse models and human blood.

Phase 1 Data

Veralox conducted two Phase 1 clinical studies of CAD-1005 in healthy volunteers; these demonstrated that CAD-1005 was well tolerated, with no deaths, no serious adverse events, and no trend in adverse event reporting with increasing doses. The first was a 2-part, placebo-controlled, study of the safety, tolerability, and pharmacokinetics (“PK”) of single and multiple ascending doses of IV CAD-1005 in 96 healthy subjects. In this study CAD-1005 was found to be well tolerated with no reports of serious adverse events (“SAEs”), dose-limiting toxicities (“DLTs”) or discontinuations; adverse events (AEs) were infrequent and mild. There were dose-linear increases in key PK metrics, approaching dose proportionality, with no upper limit on tolerability to the maximum dose tested. The second study was a Phase 1b drug-drug interaction (“DDI”) study of CAD-1005 in conjunction with argatroban. The study showed that co-administration of CAD-1005 with argatroban was well tolerated with no SAEs; AEs were infrequent and mild. Analyses of PK and PD (as measured by activated partial thromboplastin time (“aPTT”) data revealed no evidence of a pharmacokinetic or pharmacodynamic interaction

Phase 2 Data

Veralox also recently completed a Phase 2 randomized, double-blind pilot study of CAD-1005 versus placebo in participants with suspected HIT already treated with the standard of care (“SoC”) (argatroban or bivalirudin). After confirming a 4Ts score ≥ 4 and a positive PF4 immunoassay, participants were consented and enrolled; a confirmatory serotonin release assay (SRA) test was also performed, but participants were randomized and treated once the test was drawn; they did not await the test results. Participants were randomized 1:1 to either CAD-1005 plus SoC or placebo plus SoC. The study had hoped to validate a potential new surrogate endpoint for clinical efficacy, with platelet count recovery rate selected as the primary endpoint, and the composite of new or worsening thromboembolic events as the key secondary endpoint against which the surrogate was to be validated. Notably, this was the first blinded, placebo-controlled trial in HIT ever undertaken. The study was initiated in 2024; it originally intended to enroll 60 patients and was concluded in December 2025 following the transfer of program ownership from Veralox to Cadrenal. At the time the study was terminated a total of 22 participants had received study medication (12 received CAD-1005 and 10 received placebo – all on a background of either argatroban or bivalirudin). CAD-1005 failed to meet its primary endpoint since it did not significantly affect the primary endpoint of platelet count recovery rate, but a high rate of thrombotic events (>75%) was observed in the placebo group, with fewer thrombotic events in the CAD-1005 group (50%), although the study was not powered to detect statistical significance.

Planned Pivotal Phase 3 Trial

On March 26, 2026, we completed our EOP2 meeting with the FDA and clarified a potential registrational path for our planned Phase 3 pivotal trial of CAD-1005 in patients with HIT. Our Phase 3 trial protocol will still be subject to additional information which may be set forth in the final meeting minutes from the FDA and any further comments we may receive from the FDA upon their review of the protocol.

Potential Additional Applications for 12-LOX Inhibitors

Beyond HIT, selective 12-LOX inhibition has potential applications in several high-impact disease areas with multi-billion-dollar market opportunities:

●

Acute Indications: Potential opportunities in ischemia-reperfusion injury, acute kidney injury, microvascular thrombosis, and other immune thrombocytopenias.

●

Chronic Indications: Potential opportunities in diabetes (Type 1 and Type 2), obesity, atherosclerosis, vascular inflammation, and heart failure

●

Other Indications: Potential opportunities in stored platelet preservation

Tecarfarin

Tecarfarin is a novel late-stage, reversible VKA (a warfarin replacement for patients with complex needs) designed to prevent heart attacks, strokes, and deaths due to blood clots in patients requiring chronic anticoagulation. Tecarfarin is specifically designed to overcome metabolic factors that can make warfarin less reliable. Cadrenal’s approach with respect to tecararin has been a pipeline-in-a-product approach. Tecarfarin has ODD and Fast Track designation from the FDA for the prevention of systemic thromboembolism (blood clots) of cardiac origin in patients with end stage kidney disease (“ESKD”) and atrial fibrillation (“AFib”). Tecarfarin also has ODD from the FDA for the prevention of thrombosis and thromboembolism in patients with an implanted mechanical circulatory support device, which includes LVADs, a mechanical heart pump.

Tecarfarin has been evaluated in eleven (11) human clinical trials in over 1,000 individuals (269 patients were treated for at least six months, and 129 patients were treated for one year or more). In Phase 1, Phase 2, and Phase 2/3 clinical trials, tecarfarin has generally been well-tolerated in both healthy adult subjects and patients with chronic kidney disease (“CKD”). In the Phase 2/3 trial, EMBRACE-AC, the largest tecarfarin trial with 607 patients, including those with mechanical heart valves, only 1.6% of the blinded tecarfarin subjects suffered from major bleeding, and there were no thrombotic events.

Over the course of the last twelve months, the development strategy for tecarfarin has continued to evolve. We have recently completed the manufacturing of tecarfarin drug product in accordance with current good manufacturing practices (“cGMP”) and are evaluating opportunities for additional Phase 2/3 trials for ESKD patients with atrial fibrillation and/or stable LVAD patients currently treated with warfarin.

Background

There are multiple medical conditions or clinical circumstances that require anticoagulation to prevent the development of blood clots. Despite the availability of a number of parenteral (acute) and oral (chronic) agents, there is no single perfect anticoagulant for all clinical situations, and significant treatment gaps exist in the safety, predictability, and efficacy of anticoagulant therapy in a number of high-risk circumstances. The prevailing treatment for patients requiring chronic anticoagulation includes two types of oral anticoagulants: VKAs and direct acting oral anticoagulants (“DOACs”).

Warfarin is currently the predominant VKA treatment option in the U.S. and has been in use since the early 1950s, including in patients with non-valvular AFib and in patients with valvular heart diseases with AFib. Warfarin is metabolized via the cytochrome p450 (CYP450) pathway primarily by the CYP2C9 enzyme; approximately 15% of clinically used drugs are metabolized by the same enzyme, including certain anticoagulants, antiplatelets, and non-steroidal anti-inflammatory drugs. Patients taking warfarin and on CYP2C9 interacting drugs may experience either warfarin being eliminated by the body too quickly, thereby decreasing its anticoagulation effect and increasing the risk of thrombotic complications, or warfarin being eliminated by the body too slowly, resulting in excessive risk for bleeding. Other commonly appreciated drawbacks of warfarin include a relatively narrow therapeutic range, requirements for monitoring and adjustment, slow onset (with initial paradoxical prothrombotic effects due to its early inhibition of proteins C and S), and a relatively slow offset of action (making it difficult to manage with invasive procedures), and multiple drug and food interactions.

DOACs are a form of treatment that inhibits certain blood-clotting factors. While VKAs block the synthesis of vitamin K-dependent blood clotting factors (II, VII, IX, X, protein C and protein S), DOACs block the activity of specific clotting factors. DOACs are generally more rapid in onset and offset of action than VKAs, have few strong drug-to-drug interactions and do not require INR monitoring. DOACs have been approved in the U.S. for the treatment of specific oral anticoagulation indications; however, there are a number of clinical scenarios for which DOACs are contraindicated or not recommended for use, including for anticoagulation treatment in patients with LVADs, patients with ESKD and AFib, patients with ESKD and mechanical heart valves, and patients with thrombotic APS. DOACs do not have the same broad label indication as warfarin, and there are a number of indications where VKAs continue to be the standard of care, despite their limitations.

Tecarfarin is a next-generation Vitamin K antagonist that is metabolized via the human carboxylesterase 2 (“CES2”) pathway, a different metabolic pathway than warfarin, thereby avoiding CYP450 metabolism in the liver. This CES2 pathway is abundantly distributed throughout the body, unlike CYP450, which is confined to the liver. Although it exhibits genetic variability, the variants have not been shown to significantly alter drug clearance. In contrast, patients taking multiple medications that interact with CYP2C9, or CYP3A4, or those with impaired kidney function, can experience an overload in the pathway, creating a bottleneck that often leads to insufficient clearance, which results in the unstable levels of anticoagulation, an issue well documented with warfarin use. Tecarfarin has been shown in clinical studies to result in more reliable levels of anticoagulation in certain patient subgroups.

For chronic applications, two specific patient groups for which we had focused our studying were tecarfarin are patients with ESKD and AFib and patients with LVADs. Both of these clinical circumstances are particularly challenging and provide meaningful opportunities to improve care. Additionally, DOACs like Eliquis and Xarelto have either not shown clinical benefit, or their efficacy and safety remain uncertain for both indications.

ESKD + Atrial Fibrillation

AFib is the most frequently encountered human arrhythmia, with its incidence and prevalence increasing over the last 20 years. AFib is associated with an approximate five-fold increased risk of stroke. The risk of developing AFib increases in patients with CKD. According to 2023 estimates by the Centers for Disease Control and Prevention (CDC), approximately 14% of the U.S. adult population, or 35.5 million people, have CKD. An estimated 0.33% of people in the U.S. suffer from Stage 4 CKD, and 0.14% of people in the U.S. have ESKD.

There are more than 808,000 Americans with ESKD, with approximately 68% on dialysis, according to the United States Renal Data System 2023 Annual Report. Approximately 145,000 ESKD patients also have AFib. AFib nearly doubles the anticipated mortality and increases the stroke risk by approximately fivefold in these patients. There is evidence that AFib is an independent risk factor for developing ESKD in CKD patients. Both diseases share common risk factors, including hypertension, diabetes, vascular disease, and advancing age. Cardiovascular disease contributes to more than half of all deaths among patients with ESKD. According to the 2025 Annual Data Report published by the United States Renal Data System, total Medicare spending for patients with ESKD reached $55.3 billion in 2023, accounting for approximately 4.7% of the Medicare-paid claims costs.

Patients with ESKD and AFib have very high rates of stroke and death; however, there is no standard of care for these patients since there has never been a study demonstrating the benefit of any anticoagulant. The presence of either CKD or AFib increases the risk of serious thromboembolic adverse clinical outcomes, such as stroke and death. Antithrombotic therapy is typically recommended to decrease this risk in AFib patients. Still, there are no approved treatment options for patients with ESKD and AFib, and there is no standard of care for these patients. At present, there is no evidence to support the use of any drug for the prevention of thromboembolic events in patients with ESKD and AFib.

LVAD

Anticoagulation management in patients with LVADs remains a challenge. Recent randomized controlled trials in LVAD patients have shown that currently available VKAs (warfarin) result in relatively poor-quality anticoagulation (as reflected by the TTR), despite efforts to manage anticoagulation tightly in clinical trials. The ARIES-HM3 study was designed to evaluate the need for chronic aspirin treatment in patients with the newest LVAD, the HeartMate3. The use of aspirin in LVAD patients was standard but had never been proven to be beneficial. The ARIES study randomized LVAD patients to continue aspirin, along with warfarin, versus warfarin alone. The main finding of the study revealed that aspirin is not helpful in LVAD patients; however, since all patients were receiving warfarin and had careful monitoring of the quality of anticoagulation, the study also provided the opportunity to determine if the quality of anticoagulation provided by warfarin had an impact on patient outcomes. The analysis of this carefully controlled and monitored study showed that the average TTR was only 56% with warfarin, far below the benchmark for well-controlled anticoagulation of 70%, and that, despite the superior design of the HM3 device, poor quality anticoagulation was associated with excess thrombotic and bleeding events.

In March of 2025, we announced the signing of a Collaboration Agreement with Abbott Global Enterprises Limited (“Abbott”) to support the development of tecarfarin in patients with an implanted HeartMate 3 LVAD. Under the terms of the Collaboration Agreement Abbott will support us on the planning and execution of the TECarfarin Anticoagulation and Hemocompatibility with Left Ventricular Assist Devices (TECH-LVAD) trial to evaluate the efficacy and safety of tecarfarin in patients with LVADs. Under the Collaboration Agreement, Abbott will share insights from recent HeartMate trials and will support us with: trial design, site identification, trial awareness, and HeartMate expertise.

Tecarfarin Clinical Trial Summary

Tecarfarin has been evaluated in eleven (11) human clinical trials in over 1,000 individuals (269 patients were treated for at least six months and 129 patients were treated for one year or more). In Phase 1, Phase 2 and Phase 2/3 clinical trials conducted by third-parties, tecarfarin has generally been well-tolerated in both healthy adult subjects and in patients with CKD.

The Phase 2/3 EMBRACE-AC study, which was conducted by the company that owned the rights to tecarfarin at the time of the trial, was a Phase 2/3 trial multi-center, randomized, double-blind, parallel group, active control trial that compared tecarfarin to warfarin in 607 patients with indications for chronic anticoagulation, with a primary endpoint of TTR, which quantifies the percentage of INR values that are in the appropriate target range for an individual patient.

Study flow diagram for EMBRACE AC (Whitlock RP et al. Thromb Haemost 2016; 116(02): 241-250)

Dosing of study drugs was managed by a centralized dose control center. As a result of this aggressive management, the TTRs in this study were higher than in general practice. A stable dose of tecarfarin, defined as 10 % variation in weekly dose for three consecutive weeks while the INR stays within the therapeutic range, was attained in 94.5 % (290/307) of the tecarfarin patients during the study. There were no differences in the frequency of significant deviations either below (tecarfarin 2.9 % vs warfarin 3.5 %, p = 0.19) or above (tecarfarin 2.0 % vs warfarin 2.3 %, p = 0.39) the targeted therapeutic range seen between treatment groups.

The trial did not meet its primary endpoint; the mean TTR with tecarfarin (the primary endpoint) was numerically higher but not significantly superior to warfarin in terms of the primary endpoint (72.3% with tecarfarin vs 71.5% with warfarin; p=0.51), but numerically virtually all subgroups favored tecarfarin, which was especially noteworthy given the aggressiveness of INR management in the warfarin group. As part of its original analysis plan, EMBRACE-AC also included analyses of INR measurements while patients were temporarily off their trial drug due to other medical reasons. In a subsequent post-hoc analysis excluding these INR values while off therapy, the number of INR values in the therapeutic range was significantly higher on tecarfarin (68.8%) than on warfarin (66.4%) (p<0.04).

% TTR and % INR Values in therapeutic Range in EMBRACE AC

Tecarfarin was well tolerated - only 1.6% of the tecarfarin subjects had major bleeding and there were no thrombotic events. When thrombotic and major bleeding events were combined, there was a numerical imbalance (but not statistical significance) favoring tecarfarin over warfarin was seen (warfarin 11 subjects, 3.6%; tecarfarin subjects, 1.6%).

In EMBRACE-AC there were comparable rates of treatment emergent adverse events (“TEAEs”) (all adverse events observed, regardless of relationship to study drug) between the two treatment groups. TEAEs were reported for 93.2% of patients who received tecarfarin and 90.5% of patients who received warfarin. TEAEs reported by ≥10% of patients in either treatment group were nasopharyngitis (18.6% and 19.3%, blinded tecarfarin and warfarin, respectively), contusion (15.6% and 14.8%, respectively), epistaxis (8.1% and 11.1%, respectively), upper respiratory tract infection (10.7% and 10.8%, respectively), diarrhea (10.1% and 9.2%, respectively) and headache (10.7% and 8.9%, respectively). Most TEAEs were mild (32.2%, tecarfarin and 30.2%, warfarin) or moderate (45.0% and 46.6%, respectively) in severity.

Five patients died during the trial, with four deaths occurring during the double-blind period: one patient (tecarfarin; off drug) died due to mantle cell lymphoma, pneumonia and sepsis; one patient (tecarfarin; on drug) died due to cardiorespiratory arrest and myocardial infarction; one patient (warfarin; off drug) died due to metastatic colon cancer; one patient (warfarin; off drug) died due to lung cancer; and one patient (not randomized) died due to intracerebral hemorrhage. The patient who died due to intracerebral hemorrhage was considered to be possibly related to the study drug, but the remaining four deaths were not attributed to the drug. During the blinded period of the trial, five patients on tecarfarin and six patients on warfarin experienced major bleeding events. The occurrence of major bleeding events for both tecarfarin and warfarin was lower when compared to prior anticoagulation trials. Among warfarin-treated patients, there were five thrombotic events (two ischemic strokes, two deep vein thromboses and one pulmonary embolism), while there were no such events among tecarfarin-treated patients.

In a subsequent Phase 1 single-dose study comparing 13 patients with Stage 4 CKD and 10 healthy volunteers, the metabolism of warfarin was shown to be significantly inhibited, whereas tecarfarin metabolism was not altered, in the setting of significant renal insufficiency.

Frunexian

Background

Epidemiological data and studies in established animal models suggest that Factor XIa could have a substantially more significant effect on thrombosis than in hemostasis (preventing bleeding in response to an injury). Patients with plasma Factor XI levels in the top 10% of the normal range are more than twice as likely to develop deep venous thrombosis as everyone else in the study population, with a dose-response relationship between Factor XI levels and the potential for venous thrombosis. There is also an association between high plasma Factor XI levels with increased incidences of myocardial infarction and stroke. In contrast, Factor XI-deficient individuals exhibit no significant reduction in the rate of acute myocardial infarctions as compared to those with normal Factor XI levels, but have a greater than eight-fold reduction in ischemic stroke and a statistically significant reduced incidence of venous thromboembolism. Importantly, unlike hemophilia A or B, Factor XI deficiency (Hemophilia C) rarely presents as spontaneous bleeding, though in some patients, greater-than-expected blood loss is noted after trauma, surgery, or other challenges to hemostasis.

Small molecule inhibitors bind reversibly to the active site of Factor XIa and block its activity. Small-molecule Factor XI inhibitors are synthetic compounds characterized by a relatively low molecular weight, predictable potency, metabolic stability, membrane permeability, and oral bioavailability. Frunexian is unique in being the only small molecule that is administered by continuous IV infusion and being developed for acute clinical settings.

Frunexian is a highly potent, rapid-onset, selective small molecule inhibitor of Factor XIa, that inhibits factor XIa activity in a dose-proportional fashion, with a close correlation between plasma concentration of frunexian and changes in aPTT over time, and no appreciable changes in prothrombin time (“PT”). The PK and PD characteristics of frunexian — with a rapid onset of action, stable, predictable effect on coagulation, short pharmacodynamic half-life, and apparent lack of dependence on renal clearance mechanisms—appear well-suited for use in a critical care environment. Overall, frunexian administered as a single intravenous bolus or with continuous infusions over five consecutive days in healthy subjects has been generally well tolerated, and the adverse event profile did not suggest any increased risk of bleeding events.

Frunexian is the only IV small molecule Factor XIa antagonist in active development for acute indications at this time. In vivo animal studies have been conducted with frunexian to demonstrate the ability of the molecule to inhibit thrombosis, as measured by clot size and an increase in aPTT, while minimizing the risk of unwanted bleeding, as shown by the observation of no significant change in PT.

Phase 1 Studies

There are two completed Phase 1 studies with frunexian.

The first study was a placebo-controlled, randomized, double-blind, SAD/MAD study in healthy male and female subjects evaluating the safety, tolerability, PK and PD of frunexian following IV administration of single doses, via bolus injection, and multiple doses, via continuous infusion. There was a marked dose-proportional increase in the aPTT for both single dose and continuous multiple doses. In Part A frunexian was generally well tolerated when administered as single bolus IV doses of 0.01, 0.03, 0.1, 0.3, and 1.0 mg/kg. In Part B frunexian was also generally well tolerated when administered as a 24-hour continuous IV infusion over five consecutive days at doses of 0.01, 0.03, 0.1, 0.3, and 0.6 mg/kg/h. There were no SAEs. No bleeding or fluid loss was reported at the injection site. The score for bruising and bleeding at the blood sampling site was also zero at the majority of time points.

The second study evaluated higher doses of frunexian in a single-center, randomized, partially blinded, placebo-controlled, and comparator-controlled study of the safety, tolerability, PK, and PD of frunexian administered intravenously over a 5-day period in 54 healthy subjects. The main objective of the study was to extend the findings of the original Phase 1 study to evaluate the higher doses of frunexian which might be used for procedural anticoagulation. The study was blinded for frunexian dose and placebo and was open-label for subjects receiving the heparin comparator infusion. When frunexian was administered for five days, there was a strong linear relationship between exposure and dose of frunexian. After infusion, the blood concentration of frunexian decreased rapidly. PD biomarkers (aPTT, PT and activated clotting time) and their ratios/changes from baseline showed that aPTT was significantly prolonged with increasing doses of frunexian after five consecutive days of IV infusion.

A total of 54 subjects were entered into the safety data set. Excluding the TEAEs of prolonged aPTT (expected with frunexian), the incidence of TEAE during the study period was 52.5% in the frunexian group, 100% in the heparin comparator group, and 30.0% in the placebo group. TEAEs related to study drugs occurred in 10.0% of the frunexian group, 100% of the heparin group, and 10.0% of the placebo group. The TEAE associated with frunexian treatment was primarily abnormal liver function (10.0%). In the frunexian group, there was one case (2.5%) with a grade 2 infusion site reaction (1.5mg/kg/h group).

Veralox Purchase Agreement

On December 10, 2025, we entered into the Veralox Purchase Agreement pursuant to which Veralox sold to us all, or substantially all, of its right title and interest in the Veralox Assets. The Veralox Assets also included the assignment of the Old Dominion License Agreement. See, “License Agreement with Old Dominion” below for a more detailed description of the Old Dominion License Agreement. The purchase price for the Veralox Assets consisted of (i) a cash payment of $200,000, (ii) the assumption of certain assumed liabilities by us; (iii) contingent milestone payments in an amount not to exceed $15 million, and (iv) royalty payments. The transactions contemplated by the Veralox Purchase Agreement were consummated on December 10, 2025.

The contingent milestone payments, which are payable in cash, common stock, or in any combination thereof in our sole discretion, are payable upon the achievement of the following clinical and regulatory milestone events:

(i)

$2,000,000 upon the occurrence of the dosing of the first patient enrolled in the first clinical trial initiated after the closing of the transaction for CAD-1005;

(ii)

$8,000,000 upon approval of the first regulatory filing seeking approval to market a pharmaceutical product for human use containing a Compound that is covered by a patent owned or licensed by Veralox (the “Product”) in the United States;

(iii)

$2,000,000 upon approval of the first regulatory filing seeking approval to market a Product outside the United States;

(iv)

$2,000,000 upon approval of a regulatory filing seeking approval to market a Product for a subsequent indication in the United States; and

(v)

$1,000,000 upon approval of a regulatory filing seeking approval to market a Product for a subsequent indication outside the United States.

We will pay Veralox royalties of 5% on the Annual Net Sales (as such term is defined in the Veralox Purchase Agreement) of each Product containing any of the Compounds that are the subject of the Veralox Purchase Agreement which are covered by a Valid Patent Claim (as such term is defined in the Veralox Purchase Agreement) in any country, such royalty to be payable from the first commercial sale of the Product in each country until the expiration of the last-to-expire Valid Patent Claim that would be infringed by the commercialization of such Product in that country, provided however that, on a Product-by-Product and country-by-country basis, in the event that, with respect to a Product in a country, Generic Competition (as such term is defined in the Veralox Purchase Agreement) exists with respect to such Product in such country in a calendar year, then the royalty rates in such country for such Product will thereafter be reduced by fifty percent (50%). The Veralox Purchase Agreement also provides that in the event that Veralox or its affiliates licenses or otherwise acquires rights from one or more third-parties in order to make, use, sell, import or otherwise exploit a Product in a country, then 50% of any amounts payable to the third-party in such country shall be deductible from the royalty amounts payable to Veralox.

The Veralox Purchase Agreement contains customary representations, warranties and agreements by us and Veralox, customary conditions to closing, and other obligations of the parties. Subject to certain customary limitations, Veralox agreed to indemnify us, our affiliates and each of our respective successors, assigns, officers, directors, shareholders, partners, employees and agents against certain losses related to, among other things, breaches of Veralox’s representations, warranties and covenants contained in the Veralox Purchase Agreement, as well as any retained liabilities or excluded assets described therein. Subject to certain customary limitations, we also agreed to indemnify Veralox, its affiliates and each of their respective successors, assigns, officers, directors, shareholders, partners, employees and agents against certain losses related to, among other things, breaches of our representations, warranties and covenants as well as any assumed liabilities.

License Agreement with Old Dominion University

Pursuant to the Old Dominion License Agreement, the Licensor granted Veralox an exclusive worldwide license under the EVMS Patent Rights (as such term is defined in the Old Dominion License Agreement) related to the development and commercialization of 12-LOX. Veralox agreed to pay Licensor certain royalties and certain milestone payments related to the first Licensed Product or Licensed Service developed, some of which were assumed by us pursuant to the terms of the Veralox Purchase Agreement. The term “Licensed Product” is defined in the Old Dominion License Agreement as any process or method, material, composition, drug or other product, the manufacture, use or sale of which by Veralox, its affiliates or sublicensees would constitute, but for the license granted to Seller pursuant to the Old Dominion License Agreement, an infringement of any Valid Claim (as such term is defined in the Old Dominion License Agreement) of any of the EVMS Patent Rights. The term “Licensed Service” is defined in the Old Dominion License Agreement as the performance on behalf of a third-party by Veralox, its affiliates or sublicensees of any method or the manufacture of any product or the use of any product or composition which would constitute, but for the license granted to Veralox pursuant to the Old Dominion License Agreement, an infringement of a Valid Claim of the EVMS Patent Rights.

Pursuant to the Old Dominion License Agreement, we will pay Licensor milestone payments in the aggregate amount of $300,000 upon regulatory approval to market a Licensed Product in: (i) Japan or the European Union; and (ii) the United States, provided however that irrespective of whether such milestones are met, such milestone payments will be due in 2031 and 2032, respectively. Additionally, we will pay to Licensor royalties of 2% on worldwide net sales of a Licensed Product or Licensed Service less than or equal to $200,000,000 and royalties of 3% on worldwide sales greater than $200,000,000. Regardless of the commercialization status of any Licensed Product or Licensed Service, the Old Dominion License Agreement requires a minimum annual royalty payment to be paid to Licensor within (30) days of May 1^st of each year beginning May 1, 2025, ranging between $10,000 and $50,000 per year. Such annual royalty payments have been waived by Licensor for fiscal years 2026, 2027 and 2028, with the first payment to be made by us due May 1, 2029.

The Old Dominion License Agreement may be terminated: (i) upon the failure of a party to perform any material obligation required of it to be performed under the Old Dominion License Agreement and thereafter such failure to perform is not timely cured, by the non-defaulting party upon written notice; (ii) by either party upon the bankruptcy or insolvency of the other party upon written notice: (iii) by us with or without Cause (as such term is defined in the Old Dominion License Agreement) upon 90 days’ written notice to Licensor; and (iv) by Licensor: (a) in the event we fail to meet any of the Milestone Deadlines (as such term is defined in the Old Dominion License Agreement) upon 90 days’ written notice; or (b) immediately in the event we or any of our affiliates brings, or assists others in bringing, a Patent Challenge (as such term is defined in the Old Dominion License Agreement) against Licensor or any co-owner of the EVMS Patent Rights.

The foregoing descriptions of the Veralox Purchase Agreement and Old Dominion License Agreement do not purport to be complete and are qualified in their entirety by reference to the Veralox Purchase Agreement and Old Dominion License Agreement, copies of which are filed as exhibits to this Annual Report and are incorporated by reference herein.

eXIthera Purchase Agreement

On September 12, 2025, we entered into an asset purchase agreement (the “eXIthera Purchase Agreement”) with eXIthera Pharmaceuticals, Inc. (“eXIthera”), to acquire its assets, including its proprietary portfolio of investigational IV and oral Factor XIa inhibitors, including the compounds known as frunexian (EP-7041) and EP-7327 and certain other compounds, as well as all intellectual property, regulatory filings (including two inactive Investigational New Drug Applications filed with the FDA), clinical and non-clinical data, Chemistry, Manufacturing, and Controls materials, drug substance inventory, books and records, and the exclusive license agreement (the “Haisco License Agreement”) with Sichuan Haisco Pharmaceutical Co., Ltd. (“Haisco”), which relates to development of eXIthera’s lead asset, frunexian, in the Chinese market (the “eXIthera Assets”). The purchase price for the eXIthera Assets consisted of (i) $50,000 of transaction closing costs, (ii) the assumption of specific assumed liabilities related to post-closing obligations arising from the Haisco License Agreement, (iii) certain milestone payments, and (iv) royalty payments. The transactions contemplated by the eXIthera Purchase Agreement were consummated on September 12, 2025.

We have agreed to pay milestone payments to eXIthera in the aggregate amount of up to $15 million, payable in cash or in shares of our Common Stock in our sole discretion, upon the achievement of certain clinical and regulatory milestone events. The contingent milestone payments are payable upon the achievement of the following clinical and regulatory milestone events:

(i)

$500,000 upon the occurrence of the first patient dosed in first Phase 2 study initiated after the closing of the transaction with respect to frunexian or an Other IV Compound (as such term is defined in the eXIthera Purchase Agreement);

(ii)

$500,000 upon the occurrence of the first patient dosed in first Phase 1 study initiated after the closing of the transaction with respect to EP-7327 or an Other Oral Compound (as such term is defined in the eXIthera Purchase Agreement);

(iii)

$1,000,000 upon the occurrence of the first patient dosed in first Phase 3 study initiated after the closing of the transaction with respect to frunexian or an Other IV Compound;

(iv)

$1,000,000 upon the occurrence of the first patient dosed in first Phase 3 study initiated after the closing of the transaction with respect to EP-7327 or an Other Oral Compound);

(v)

$6,000,000 on the date the FDA grants approval of a New Drug Application (“NDA”) for frunexian or an Other IV Compound;

(vi)

$6,000,000 on the date the FDA grants approval of an NDA for EP-7327 or an Other Oral Compound.

We are obligated to pay eXIthera and its assignees, a royalty equal to 2% of the Annual Net Sales (as such term is defined in the eXIthera Purchase Agreement) of pharmaceutical products containing any of the Compounds that are the subject of the eXIthera Purchase Agreement which are covered by a valid patent in any country except China, such royalty to be payable from the first commercial sale of a product in each country until the later of: (a) expiration of the last-to-expire Valid Patent Claim (as such term is defined in the eXIthera Purchase Agreement) that would be infringed by the commercialization in that country, (b) expiration of regulatory exclusivity in that country (including when generic competition occurs), or (c) ten years from the first commercial sale of the product in that country.

Additionally, we are obligated to pay eXIthera 50% of all royalties actually received by us from Haisco under the existing Haisco License Agreement, without any limitations on the total amount paid or the time period within which such payments will be made. We also agreed to assume only post-closing obligations arising from the Haisco License Agreement, but only to the extent that such obligations do not arise from any breach or default by eXIthera under the Haisco License Agreement on or before the closing of the transaction.

SEC Form 10-K filed by Cadrenal Therapeutics Inc.