UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 10-Q

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

For the quarterly period ended June 30, 2026

or

☐ 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: 001-38323

ADIAL PHARMACEUTICALS, INC.

(Exact Name of Registrant as Specified in its Charter)

(804) 487-8196

Registrant’s Telephone Number, Including Area Code

Former Name, Former Address and Former Fiscal Year, if Changed Since Last Report

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

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, 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.

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 is a shell company (as defined in Rule 12b-2 of the Act). Yes ☐ No ☒

Number of shares of common stock outstanding as of August 12, 2026 was 2,625,890.

ADIAL PHARMACEUTICALS, INC.

NOTE REGARDING FORWARD-LOOKING STATEMENTS

This Quarterly Report on Form 10-Q 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”). In particular, statements contained in this Quarterly Report on Form 10-Q, including but not limited to, statements regarding the sufficiency of our cash, our ability to finance our operations, and business initiatives and to obtain funding for such activities; our future results of operations and financial position, business strategy and plan prospects costs and objectives of management for future acquisitions, and expected changes to our business, results of operations, management team and board of directors in connection with our recent acquisition of Azora Therapeutics, Inc. are forward looking statements. These forward-looking statements relate to our future plans, objectives, expectations and intentions and may be identified by words such as “may,” “will,” “should,” “expects,” “plans,” “anticipates,” “intends,” “targets,” “projects,” “contemplates,” “believes,” “seeks,” “goals,” “estimates,” “predicts,” “potential” and “continue” or similar words. Readers are cautioned that these forward-looking statements are based on our current beliefs, expectations and assumptions and are subject to risks, uncertainties, and assumptions that are difficult to predict, including those identified below, under Part II, Item lA. “Risk Factors” and elsewhere in this Quarterly Report on Form 10-Q and those risks identified under Part I, Item 1A of our Annual Report on Form 10-K for the year ended December 31, 2025 filed with the Securities and Exchange Commission (the “SEC”) on March 5, 2026 (“2025 Form 10-K”). Therefore, actual results may differ materially and adversely from those expressed, projected or implied in any forward-looking statements. We undertake no obligation to revise or update any forward-looking statements for any reason.

NOTE REGARDING COMPANY REFERENCES

Throughout this Quarterly Report on Form 10-Q, “Adial,” the “Company,” “we,” “us” and “our” refer to Adial Pharmaceuticals, Inc.

FORM 10-Q

TABLE OF CONTENTS

PART I – FINANCIAL INFORMATION

Item 1. Condensed Consolidated Unaudited Financial Statements

ADIAL PHARMACEUTICALS, INC.

CONDENSED CONSOLIDATED BALANCE SHEETS (UNAUDITED)

(In thousands, except share and per share amounts)

The accompanying notes are an integral part of these unaudited condensed consolidated financial statements.

ADIAL PHARMACEUTICALS, INC.

CONDENSED CONSOLIDATED STATEMENTS OF OPERATIONS (UNAUDITED)

(In thousands, except share and per share amounts)

The accompanying notes are an integral part of these unaudited condensed consolidated financial statements.

ADIAL PHARMACEUTICALS, INC.

CONDENSED CONSOLIDATED STATEMENTS OF TEMPORARY EQUITY

AND STOCKHOLDERS’ (DEFICIT) EQUITY (UNAUDITED)

(In thousands, except share amounts)

The accompanying notes are an integral part of these unaudited condensed consolidated financial statements.

ADIAL PHARMACEUTICALS, INC.

CONDENSED CONSOLIDATED STATEMENTS OF CASH FLOWS (UNAUDITED)

(In thousands)

The accompanying notes are an integral part of these unaudited condensed consolidated financial statements.

ADIAL PHARMACEUTICALS, INC.

NOTES TO UNAUDITED CONDENSED CONSOLIDATED FINANCIAL STATEMENTS

Item 2. Management’s Discussion and Analysis of Financial Condition and Results of Operations.

The following discussion and analysis is intended as a review of significant factors affecting our financial condition and results of operations for the periods indicated. The discussion should be read in conjunction with our unaudited condensed consolidated financial statements and the notes presented herein included in this Form 10-Q and the audited consolidated financial statements and the other information set forth in the Annual Report on Form 10-K for the year ended December 31, 2025 that we filed with the SEC on March 5, 2026 (the “2025 Form 10-K”). ln addition to historical information, the following Management’s Discussion and Analysis of Financial Condition and Results of Operations contains forward-looking statements that involve risks and uncertainties including, but not limited to, those set forth below under “Risk Factors” and elsewhere herein, and those identified under Part I, Item 1A of the 2025 Form 10-K. Our actual results could differ significantly from those anticipated in these forward-looking statements as a result of certain factors discussed herein and any other periodic reports filed and to be filed with the Securities and Exchange Commission (“SEC”).

On February 5, 2026, we effected a one-for-twenty-five reverse stock split (the “Reverse Stock Split”) of our authorized, issued and outstanding common stock. Unless otherwise noted, all references to share amounts in this Form 10-Q reflect the Reverse Stock Split.

Overview

We are a clinical-stage biopharmaceutical company focused on developing treatments for serious inflammatory diseases, and the development of therapeutics for the treatment or prevention of addiction and related disorders. On June 11, 2026, we completed our previously announced acquisition of Azora Therapeutics, Inc. (“Azora”), a biopharmaceutical company developing treatments for serious inflammatory diseases, pursuant to an Agreement and Plan of Merger, dated June 11, 2026 (the “Merger Agreement”), by and among Adial, Adial Merger Sub, Inc. (“First Merger Sub”), Adial Second Merger Sub, LLC (“Second Merger Sub”) and Azora. Pursuant to the Merger Agreement, First Merger Sub merged with and into Azora, with Azora surviving as a wholly owned subsidiary of Adial (the “First Merger”). Immediately following the First Merger, Azora merged with and into Second Merger Sub, with Second Merger Sub surviving as a wholly owned subsidiary of Adial and the Second Merger Sub changing its name to “Azora Therapeutics, LLC” (the “Second Merger” and, together with the First Merger, the “Merger”). . On June 12, 2026 we received approximately $24.3 million in net proceeds from the initial closing of a private placement financing from a group of institutional investors, with potential additional closings. The Merger brought Azora’s lead investigational candidate, AT177, into our pipeline. For additional information regarding the terms of the Merger and the concurrent financing, see Note 4 to the unaudited condensed consolidated financial statements included elsewhere in this Quarterly Report on Form 10-Q.

Azora has historically focused on developing aryl hydrocarbon (“AhR”) receptor agonists to treat autoimmune diseases including ulcerative colitis. Following the Merger, our focus has shifted to the treatment of serious inflammatory diseases and our lead program is AT177 being studied for the treatment of ulcerative colitis (“UC”). AT177 is a fully synthetic, patented, oral AhR agonist designed to restore mucosal immune homeostasis at the site of disease with minimal systemic exposure. Its active ingredient is a prodrug of indirubin, the most potent AhR agonist within indigo naturalis, a botanical extract with best-in-category clinical efficacy in ulcerative colitis. AT177’s colon-targeted formulation delivers therapeutic AhR engagement directly to the colonic mucosa with exquisite gut restriction, minimizing the systemic AhR exposure associated with adverse effects. In preclinical studies, AT177 demonstrated robust local colonic AhR activation with markedly limited systemic exposure and superior colon-to-systemic selectivity compared to other AhR agonists in development. AT177 is currently in IND-enabling studies, with an investigational new drug (“IND”) filing planned for the second quarter of 2027, initiation of a Phase 1a single- and multiple-ascending-dose (“SAD/MAD”) clinical trial planned to commence in the second half of 2027, followed by a Phase 1b proof-of-concept study in UC patients.

Prior to the Merger, we were primarily focused on the development of AD04, a genetically targeted, serotonin-3 receptor antagonist, therapeutic agent for the treatment of Alcohol Use Disorder (“AUD”) in heavy drinking patients. Historically, we have devoted the vast majority of our resources to development efforts relating to AD04, including preparation for and conducting clinical trials, providing general and administrative support for these operations and protecting our intellectual property.

We currently do not have any products approved for sale and we have not generated any significant revenue since our inception. From our inception through the date of this Quarterly Report on Form 10-Q, we have funded our operations primarily through the private and public placements of debt, equity securities, and an equity line.

Our current cash and cash equivalents, are not expected to be sufficient to fund operations for the twelve months from the date of filing this Quarterly Report on Form 10-Q, based on our current commitments and development plans. We have incurred recurring losses and need to raise additional funds to sustain our operations. These factors raise substantial doubt about our ability to continue as a going concern.

We have incurred net losses in each year since our inception, including net losses of approximately $54.0 million, inclusive of the one-time acquired in process research and development write off of $46.2 million, and $8.0 million for the six months ended June 30, 2026 and year ended December 31, 2025, respectively. We had accumulated deficits of approximately $144.0 million and $90 million as of June 30, 2026 and December 31, 2025, respectively. All of our operating losses in the six months ended June 30, 2026 resulted from costs incurred in operations, including costs in connection with our continuing research and development programs and from general and administrative costs associated with our operations.

We will not generate revenue from product sales unless and until we successfully complete development and obtain marketing approval for AT177 or AD04, which we expect will take a number of years and is subject to significant uncertainty.

Until such time, if ever, as we can generate substantial revenue from product sales, we expect to finance our operating activities through a combination of equity offerings, debt financings, government or other third-party funding, commercialization, marketing and distribution arrangements and other collaborations, strategic alliances and licensing arrangements. However, we may be unable to raise additional funds or enter into such other arrangements when needed on favorable terms or at all. Our failure to raise capital or enter into such other arrangements as and when needed would have a negative impact on our financial condition and our ability to develop AT 177 and AD04. 

Recent Developments

Acquisition of Azora

On June 11, 2026, we acquired Azora in accordance with the terms of the Merger Agreement. Pursuant to the Merger Agreement, Azora became a wholly owned subsidiary of the Company.

At closing of the Merger, we issued to former Azora stockholders 437,421 shares of our common stock and 12,930.617 shares of Series A Non-Voting Convertible Preferred Stock, par value $0.001 per share (“Series A Preferred Stock”). Each share of Series A Preferred Stock is convertible into 1,000 shares of our common stock, subject to the terms and limitations set forth in the applicable certificate of designation and related transaction documents, including without limitation the receipt of approval of our stockholders of the conversion thereof. Azora outstanding options to purchase Azora common stock were converted into options to purchase an aggregate of 1,177,782 shares of our common stock.

On June 11, 2026, in connection with, and as a condition to closing of, the Merger, we entered into a Securities Purchase Agreement (the “Purchase Agreement”) with the purchasers named therein (the “PIPE Investors”), pursuant to which we issued and sold to the PIPE Investors, in a private placement transaction, at the initial closing on June 12, 2026 (the “Initial PIPE Closing”), pre-funded warrants (the “Initial Closing Pre-Funded Warrants”) to purchase up to an aggregate of 9,749,345 shares of common stock, at a price of $2.7489 per Initial Closing Pre-Funded Warrant), for an aggregate purchase price of $26.8 million. In addition, we agreed to issue and sell to the PIPE Investors, at one or more subsequent closings (each, a “Milestone Closing”), pre-funded warrants (“Milestone Pre-Funded Warrants”) to purchase up to an aggregate of 9,749,345 shares of common stock and incentive warrants (“Milestone Incentive Warrants” and, together with the Milestone Pre-Funded Warrants, the “Milestone Warrants”) to purchase up to an aggregate of 9,749,345 shares of common stock, at a combined purchase price equal to $2.7489 per Milestone Warrants, for an aggregate purchase price of up to $26.8 million. The issuance and sale of Initial Closing Pre-Funded Warrants and Milestone Warrants pursuant to the Purchase Agreement are collectively referred to as the “Financing.”

Pursuant to the terms of the Merger Agreement, upon the closing of the Merger, we agreed to guarantee the payment of $5.5 million in principal amount of certain amended and restated convertible promissory notes issued by Azora (the “Azora Notes”) to certain individuals (collectively, the “Former Azora Noteholders”). On June 11, 2026, we entered into exchange agreements (the “Exchange Agreements”) with the Former Azora Noteholders to extinguish the payment guaranty and retire the Azora Notes in exchange for the issuance to the Former Azora Noteholders of Initial Closing Pre-Funded Warrants to purchase an aggregate of 2,031,603 shares of common stock (the “Azora Note Exchange”). As a result of the Azora Note Exchange, all such Azora Notes have been deemed to be repaid in full and all outstanding obligations thereunder have been extinguished. Pursuant to the Exchange Agreements, the Former Azora Noteholders are also entitled to participate in Milestone Closings to purchase Milestone Pre-Funded Warrants to purchase up to an aggregate of 2,031,603 shares of common stock and Milestone Incentive Warrants to purchase up to an aggregate of 2,031,603 shares of common stock, at a combined price of $2.7489, on substantially the same terms as the PIPE Investors under the Purchase Agreement, for an aggregate purchase price of up to $5.6 million. We accounted for the Azora Note Exchange as a debt extinguishment and an extinguishment loss of $6.1 million was recognized based upon the difference between the reacquisition price and the net carrying amount of the Azora Notes. The reacquisition price is equal to the fair value of the Initial Closing Pre-Funded Warrants to purchase an aggregate of 2,031,603 shares of Adial’s common stock and the liability classified rights to participate in Milestone Closings to purchase Milestone Pre-Funded Warrants to purchase up to an aggregate of 2,031,603 shares of Adial’s common stock and Milestone Incentive Warrants having an exercise price of $2.7489 per share to purchase up to an aggregate of 2,031,603 shares of Adial’s common stock issued upon the Azora Note Exchange and the net carrying amount is equal to the principal and accrued interest amount of the Azora Notes.

The Azora Note Exchange, together with the Merger and the Financing, are referred to as the “Transactions.”

Our Product Candidates

Azora is developing colon-targeted AhR agonists for the treatment of inflammatory bowel disease (“IBD”). Azora was originally incorporated as Meya Pharmaceuticals and later renamed and co-founded by Matthew Davidson, Ph.D., Julie Saiki, Ph.D., and Johan Andreasson Ph.D., and was spun out of Stanford University’s translational medicine SPARK program. In connection with the Merger, Dr. Davidson, Azora’s co-founder and former Chief Executive Officer, was appointed as our Chief Development Officer and as a member of our Board of Directors, Dr. Saiki was appointed Executive Vice President of Strategy. and Wendy Young, Ph.D., formerly Senior Vice President of Small Molecule Drug Discovery at Genentech, was appointed to our Board of Directors as an independent director upon closing of the Merger.

AhR is a master regulator of gut immune and epithelial barrier function and restoring AhR signaling at the intestinal mucosa has been clinically validated as a mechanism for treating UC. Our core scientific thesis is that delivering potent, localized AhR agonism directly to the colon, while minimizing systemic exposure, can capture the efficacy of AhR activation demonstrated in patients while mitigating the systemic safety liabilities observed with previous generations of AhR agonists.

AT177 was inspired by indigo naturalis, a botanical extract with demonstrated clinical benefit in UC but with certain limitations inherent to an uncontrolled botanical. AT177 is a rationally designed prodrug that liberates indirubin, the most potent AhR agonist in indigo naturalis, directly in the colon in a controlled, fully-synthetic, patented oral dosage form. We believe AT177 has the potential to be a differentiated treatment for UC. As of the date of this Quarterly Report on Form10-Q, we have completed a GLP toxicology in rats evaluating AT177, received pre-IND feedback from the U.S. Food and Drug Administration (the “FDA”), and are advancing AT177 through IND-enabling studies, with an IND planned for the second quarter of 2027. We intend to advance AT177 into a Phase 1a SAD/MAD study followed by a Phase 1b proof-of-concept (“PoC”) study in patients with UC, with an initial proof-of-concept readout anticipated in first half of 2028.

In addition to AT177, our pipeline includes AD04, our legacy investigational product candidate for the treatment of AUD, which is described under “Legacy Program — AD04,” below.

Our Pipeline

Figure: Our pipeline — AT177 in UC (lead), AT177 in Crohn’s disease, and an undisclosed platform program. Source: Company materials.

Corporate Strategy

Our mission is to improve the lives of patients suffering from serious inflammatory diseases by developing differentiated therapies that restore immune balance at the site of disease. Our strategy to achieve this goal centers on the following development priorities:

Ulcerative Colitis and the Case for Colon-Targeted AhR Agonism

Disease Overview and Unmet Need

UC is a chronic inflammatory bowel disease characterized by inflammation and ulceration of the colonic mucosa. Symptoms include rectal bleeding, urgency, diarrhea and abdominal pain and can severely impact quality of life. Ulcerative colitis arises from a dysregulated immune response, with immunologic, epithelial barrier and environmental factors all contributing to disease initiation and progression. It is estimated that UC and Crohn’s disease impacts more than 5.0 million patients worldwide and growing.

In the United States, approximately 1.25 million patients were treated for UC in 2020, representing an estimated U.S. total addressable market of approximately $8.4 billion in 2023 and growing. Despite meaningful therapeutic advances over the last decade, including more than 15 approved therapies across multiple classes, UC continues to impose a substantial burden of illness, with clinical remission at induction rates generally below 30% and durable mucosal healing remaining a central unmet clinical priority.

Despite the availability of multiple classes of approved therapies, UC remains an area of substantial unmet need. Existing therapies are limited by:

As a result, there remains a significant need for an oral therapy that achieves high, durable rates of remission with a favorable safety profile. We designed AT177 with the goal of addressing these limitations.

The Aryl Hydrocarbon Receptor (AhR) Is a Master Regulator of Gut Health

The AhR is a ligand-activated transcription factor expressed in immune cells and intestinal epithelial cells that regulates both immune function and epithelial barrier integrity. Polymorphisms in AhR have been associated with increased risk of UC. AhR agonism has been shown to reduce pro-inflammatory cytokines, including IL-17a, IL-6 and TNFα, to increase the anti-inflammatory and tissue-protective cytokines IL-10 and IL-22 and regulatory T cells (Tregs), and to increase expression of tight junction proteins. By restoring barrier function locally, AT177 may help end the cycle whereby additional bacteria, antigens and inflammatory triggers can enter the body via a disrupted mucosal barrier and further exacerbate the ongoing immune response. We believe that AT177 can be used in combination with existing targeted drugs for UC, given its orthogonal mechanism.

Systemic AhR agonists have demonstrated efficacy in UC and other inflammatory diseases, providing clinical validation of the target. However, systemic AhR signaling has been associated with potential safety risks, including headaches, cardiovascular adverse events, and systemic immunosuppression that may increase risk of malignancy. These observations informed our strategy of delivering potent AhR agonism locally in the colon while minimizing systemic exposure.

Figure: The AhR is a master regulator of gut immune and epithelial barrier function. Source: Company materials.

Indigo Naturalis Supports Validation of the AhR Mechanism in Ulcerative Colitis

Indigo naturalis, a botanical extract used historically in traditional medicine practices in East Asia, has demonstrated profound and durable efficacy in UC, providing clinical validation of the AhR mechanism. Our co-founder, Dr. Julie Saiki, conducted a Phase 1b study of indigo naturalis in refractory UC patients at Stanford University (Saiki et al., BMJ Open Gastroenterology, 2021; n=11), of whom 9 of 11 had failed anti-TNF therapy and 5 of 11 had been recommended for colectomy. In this study, indigo naturalis drove robust colonic AhR target engagement (~12,000-fold mean increase in colonic AhR activity). This study supports validation of the AhR mechanism in UC.

The clinical benefit of indigo naturalis in UC has been demonstrated in additional studies. In a randomized, double-blind, placebo-controlled trial (Naganuma et al., Gastroenterology, 2018; n=86), indigo naturalis demonstrated up to approximately 50% placebo-adjusted clinical remission at Week 8, with benefit observed in both biologic-experienced and biologic-naïve patients. In a longer-term maintenance study (Matsuno et al., 2022; n=33), clinical remission was reported in approximately 73% of patients at one year. Despite this efficacy, indigo naturalis is an uncontrolled botanical mixture that is not FDA-approved and carries potential systemic safety liabilities, limiting its utility as a therapy.

Figure: Indigo naturalis has demonstrated profound, durable efficacy in ulcerative colitis, validating the AhR mechanism. Source: Company materials.

Efficacy Is Driven Locally, Not Systemically

Preclinical and clinical evidence supports our thesis that the therapeutic benefit of AhR agonism in UC is driven by local activation in the colonic epithelium, rather than by systemic exposure. In a chronic murine colitis model, selective deletion of AhR in intestinal epithelial cells eliminated most of the benefit of AhR agonism, supporting that colonic epithelial AhR signaling is critical to efficacy. In addition, tapinarof (Vtama®), a topically-applied AhR agonist approved for psoriasis and atopic dermatitis, achieves its therapeutic effect with minimal systemic exposure. Consistent with these findings, Azora’s fully-owned, topical indirubin program, AT193, has demonstrated activity in psoriasis with no quantifiable systemic exposure in a Phase 1b study conducted in Australia. Although the program is not in active development, the clinical data supports the hypothesis that only local activation alone is sufficient for efficacy in another autoimmune disease. Together, these data support our belief that local AhR activation is sufficient to drive clinical benefit.

AT177 — Our Lead Product Candidate

Composition and Mechanism of Action

AT177 is a fully-synthetic, gut-restricted, small-molecule prodrug designed to recapitulate the benefit of indigo naturalis while minimizing systemic exposure. AT177 converts in the colonic lumen to indirubin,, the most potent AhR agonist in indigo naturalis, in the colon. Conversion to indirubin occurs via hydrolysis across a range of physiological pHs expected in healthy and UC colons and does not rely on microbial activity or expression of enzymes which may be disrupted in UC patients. By liberating indirubin directly at the site of disease, AT177 is designed with the intention to maximize local AhR activation in the colonic epithelium while limiting systemic exposure.

Figure: AT177 converts into indirubin, the active moiety in indigo naturalis. Source: Company materials.

Differentiated Product Profile

We believe that AT177 has a differentiated clinical profile compared with approved therapies and other AhR candidates in development:

Preclinical Evidence

In a dextran sodium sulfate (“DSS”) murine colitis model, oral AT177 was effective and produced superior in vivo colonic AhR activity relative to indirubin, achieving approximately 8-fold greater local colonic AhR signaling than a molar-equivalent amount of indirubin. In a trinitrobenzene sulfonic acid (“TNBS”) murine colitis model, oral AT177 reduced disease activity and preserved colonic crypt architecture, restored epithelial integrity and reduced inflammatory infiltrate in the lamina propria on histology.

In large-animal studies, AT177 delivered indirubin at concentrations above the AhR EC50 across the entire colon and into the rectum, while maintaining dramatically lower systemic exposures than other AhR agonists, suggesting a potentially favorable therapeutic index and a gut-restricted profile.

We believe these preclinical data, together with the clinical evidence supporting the AhR mechanism from indigo naturalis studies and the shared active moiety, reduce certain development risks for AT177. However, substantial development risks remain, including risks related to safety, efficacy, manufacturing, and regulatory approval.

Competitive Positioning Among AhR Agonists

We believe that AT177’s profile is differentiated against other AhR agonists because it is highly potent, rapidly metabolized, and has an optimized pharmacokinetic/pharmacodynamic (“PK/PD”) profile for UC with robust gut-restriction. Its active moiety, indirubin, is unique in that it has demonstrated clinical benefit in patients as a component of indigo naturalis and is an endogenous molecule, characteristics that we believe may be relevant to its favorable safety and tolerability profile.

We are aware of several other parties developing drugs with AhR activity in inflammatory bowel disease, including Abivax, Equillium and Dr. Falk Pharma (in partnership with AllianThera Biopharma).

Abivax is developing obefazimod, an orally administered, medium-potency systemic AhR agonist that induces upregulation of MiR-124. Obefazimod has reported approximately 16.4% placebo-adjusted clinical remission at Week 8 at a 50 mg dose in its Phase 3 ABTECT program. Based on published data, we believe obefazimod’s PK/PD profile may not achieve optimal colonic AhR activation, with near-undetectable levels of obefazimod and its metabolite reported in rectal biopsies in a Phase 1 study.

Equillium is developing EQ504, a preclinical-stage AhR modulator that it acquired through its 2024 acquisition of Ariagen, Inc. We believe a key distinction between AT177 and EQ504 is that AT177’s active moiety, indirubin, has established clinical validation in ulcerative colitis, whereas EQ504’s active moiety has not, to our knowledge, been evaluated in patients. Further the systemic exposure due to EQ504 administration is unknown.

Dr. Falk is developing ATB102, an early clinical-stage orally administered AhR/Nrf2 agonist which appears to be based on the tapinarof scaffold. ATB102 appears to be a medium potency AhR agonist with reduced systemic exposure relative to tapinarof.

Figure: AT177 was rationally designed to be a potential best-in-class AhR agonist for ulcerative colitis. Source: Company materials.

Clinical Development Plan

Our near-term development priorities are focused on advancing AT177 efficiently through IND-enabling studies into Phase 1a safety and pharmacology studies, followed by a Phase 1b proof-of-concept trial in patients with UC. As of the date of this Quarterly Report on Form 10-Q, we have scaled drug substance, demonstrated in vivo efficacy in animal models, achieved target PK/PD in large animals, and completed GLP toxicology studies in rats. We have received pre-IND feedback from the FDA and are conducting IND-enabling studies in line with FDA guidance. Our proposed IND enabling package will include phase-appropriate toxicology studies in a rodent and non-rodent species, genotoxicity studies, safety pharmacology studies, adsorption, distribution, metabolism and excretion (“ADME”) studies, transporter studies, phototoxicity studies, pharmacology studies, and AhR binding studies. We plan to file an IND for AT177 in the second quarter of 2027 and to initiate a Phase 1a SAD/MAD study followed by a Phase 1b proof-of-concept study in UC patients, with an initial proof-of-concept readout anticipated in the first half of 2028.

Figure: Financing positions AT177 through IND-enabling studies and into clinical proof of concept in UC. Source: Company materials.

Chemistry, Manufacturing and Controls

AT177 is manufactured from commercially available, fully-synthetic starting materials using a proprietary, highly scalable synthetic route. We have completed kilogram-scale feasibility batches and have observed drug-substance stability of greater than 18 months at room temperature. We have initiated the development of U.S.-based current Good Manufacturing Practice (“cGMP”) manufacturing with a long-term development partner. The drug product is a colon-targeted oral formulation that uses only FDA-approved excipients and is designed to provide a highly targeted colonic release profile, which has been confirmed in large-animal studies. We believe AT177’s CMC package is well-positioned to support clinical advancement.

Potential Future Indications

We believe our colon-targeted AhR agonist holds promise across a broader range of immune-mediated conditions, including other inflammatory bowel diseases. A proof of concept in ulcerative colitis is intended, if successful, to unlock development of AT177 in Crohn’s disease, and we believe AT177’s mechanism is orthogonal to, and potentially combinable with, approved UC therapies. We also intend to explore additional, undisclosed platform opportunities as the AT177 program advances.

Legacy Program — AD04

Prior to the Merger, we were a clinical-stage pharmaceutical company focused on the treatment and prevention of addiction and related disorders. Our legacy investigational product candidate, AD04, was being developed as a potential therapy for alcohol use disorder, or AUD. AD04 was previously evaluated in the Phase 3 ONWARD trial for the treatment of AUD in patients with specific target genotypes identified through a companion genetic diagnostic test. See Part I, Item 1. Business of our Annual Report on Form 10-K for the year ended December 31, 2025, for additional information regarding our legacy AD04 program and additional information about our business prior to the Merger.

Competition

The biotechnology and pharmaceutical industries are characterized by rapidly advancing technologies, intense competition and a strong emphasis on intellectual property. While we believe our differentiated, colon-targeted AhR agonist approach provides a competitive advantage, we face competition from many sources, including pharmaceutical and biotechnology companies, academic institutions, governmental agencies and public and private research institutions.

The UC market in particular has become an increasingly competitive space. There are now multiple classes of approved therapies — including anti-TNF agents, anti-integrin antibodies, IL-12/23 and IL-23 inhibitors, JAK inhibitors and S1P receptor modulators — as well as numerous product candidates in clinical development. There are also several competitive AhR-directed approaches including obefazimod (Abivax), EQ504 (Equillium), ATB102 (Dr. Falk Pharma in partnership with AllianThera).

Intellectual Property

We seek to protect proprietary technology, inventions and improvements that are commercially important to the development of our business by seeking, maintaining and defending patent rights, and leveraging trade secrets, know-how and regulatory exclusivities where available.

We solely own intellectual property rights covering AT177 on a worldwide, royalty-free basis. Our granted composition-of-matter patent directed to AT177 extends to 2042. We are also pursuing patent protection for our colon-targeted AhR agonist formulations and methods of preventing or mitigating side effects (headaches, GI, PAH) and enhancing the efficacy of AhR agonists. The following table summarizes our key issued patents directed to AT177:

GI = gastrointestinal; PAH = pulmonary arterial hypertension. Patent expiration dates shown do not include any patent term extension or adjustment that may be available.

As of July 27, 2026, our patent estate related to AT177 and our broader patent families (four) are described below:

We hold these rights outright and are not subject to any third-party license, royalty or milestone obligations with respect to AT177. In addition to patent protection, we rely on trade secrets, know-how and continuing technological innovation to protect our technology. We intend to seek patent term extension under the Hatch-Waxman Act for one or more patents covering AT177 following any marketing approval, where available.

Manufacturing

We do not own or operate, and currently have no plans to establish, manufacturing facilities for the production of AT177. We rely, and expect to continue to rely, on third-party contract manufacturing organizations (“CMOs”) for our raw materials, drug substance and drug product needs for preclinical research and clinical supply, and expect to do so for any future commercial supply. AT177 is manufactured from commercially available, fully-synthetic starting materials using a proprietary, highly scalable synthetic route.

Sales and Marketing

Given our current stage of development, we have not yet established a commercial organization or distribution capabilities. If AT177 or any other product candidate receives marketing approval from the FDA, we expect to manage sales, marketing, patient access and distribution through internal resources, third-party relationships, or collaboration with one or more pharmaceutical companies to enhance our commercial capabilities.

Key Factors Impacting the Comparability of Results

The historical results of operations for the periods presented may not be comparable, either to each other or to our future results of operations, for the reasons described below:

Acquisition of Azora

On June 11, 2026, we completed the acquisition of Azora. As a result of this transaction, Azora became a wholly owned subsidiary of ours, and our business shifted from the development of AD04 for the treatment of AUD in heavy drinking patients to being primarily focused on the development of AT177 for the treatment of UC.

We have been determined to be the accounting acquirer, and accordingly, the financial statements for periods prior to the Merger reflect only the historical results of our legacy AUD focused business. The results of operations of Azora have been included in our consolidated financial statements beginning on the date of the Merger, June 11, 2026.

As a result, the results of operations for the three and six months ended June 30, 2026 include (i) our legacy AUD focused operations for the full period and (ii) the results of Azora for the period from June 11, 2026 through June 30, 2026. Accordingly, the results for the current period are not directly comparable to prior periods.

In addition, the Merger resulted in significant changes to our financial position, including the recognition of substantial in process research and development expense. We also incurred transaction-related costs and integration-related expenses in connection with the Merger, which impacted operating results for the current period.

Following the Merger, we operate with a different product candidate, cost structure, capital requirements, and personnel. As a result of these changes, period-to-period comparisons of our historical results may not be indicative of future performance.

Results of operations for the three months ended June 30, 2026 and 2025

The following table sets forth the components of our statements of operations in dollars for the periods presented (in thousands):

Research and development (“R&D”) expenses

Research and development expenses decreased by approximately $292,000 (40%) to $440,000 during the three months ended June 30, 2026 compared to $732,000 for the three months ended June 30, 2025. The decrease was mainly due to decreased CMC and decreased research and development activity as the Company was engaged in merger discussions in the three months ended June 30, 2026 as compared to the same period in 2025.

General and administrative expenses (“G&A”) expenses

General and administrative expenses increased by approximately $4,250,000 (370%) to $5,400,000 during the three months ended June 30, 2026 compared to $1,150,000 for the three months ended June 30, 2025. The increase was mainly due to merger related cost associated with the acquisition of Azora and bonus and severance expenses incurred in the three months ended June 30, 2026 as compared to the same period in 2025.

Acquired In-Process Research and Development Expense

Acquired in-process research and development expense was $46.2 million for the three months ended June 30, 2026, with no comparable expense in the prior year period. The charge was recognized in connection with the acquisition of Azora in June 2026 and represents the fair value of acquired IPR&D assets that had no alternative future use as of the acquisition date. See Note 4 to our unaudited condensed consolidated financial statement included elsewhere in this Quarterly Report on Form 10-Q for additional information regarding the Merger.

Change in Value of Equity Method Investment

The expense recognized to the change in the value of our equity method investment in Adovate, LLC (“Adovate”) increased by approximately $82,000 in the three months ended June 30, 2026 compared to the three months ended June 30, 2025. This increase is due to variations in the loss recognized related to our equity investment which includes a lower equity share, with changes to the value of our Adovate equity recognized on a three month lag.

Total Other income (expenses)

Total other income (expense), was $36,000 for the three months ended June 30, 2026, compared to ($76,000) for the same period in 2025. The change was primarily driven by a ($6.1) million non-cash loss on extinguishment of promissory notes, recognized in connection with the acquisition with Azora when we exchanged outstanding promissory notes for pre-funded warrants to purchase our common stock, ($2.1) million financing costs, offset by $8.3 million change in the fair value of our milestone warrant rights.

Total other income, excluding losses from the equity method investment, change in fair value of milestone warrant rights liability and financing costs, loss on extinguishment of promissory notes, increased by approximately $35,000 in the three months ended June 30, 2026 compared to the three months ended June 30, 2025.

Results of operations for the six months ended June 30, 2026 and 2025

The following table sets forth the components of our statements of operations in dollars for the periods presented (in thousands):