On March 12, 2026 Enodia Therapeutics, a biotechnology company developing novel small-molecule therapies for targeted protein degradation at the point of synthesis, and Kezar Life Sciences, Inc. (Nasdaq:KZR), a clinical-stage biotechnology company developing novel small molecule therapeutics to treat unmet needs in immune-mediated diseases, reported that Enodia has acquired Kezar’s assets from its Sec61-based discovery and development program. The acquisition enables Enodia to advance its understanding of Sec61 selectivity mechanisms, expanding biological and translational insights for faster progression toward key clinical milestones.

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Under the terms of the purchase agreement between Enodia and Kezar, Kezar will receive an initial upfront payment totaling $1 million, and will receive future payments upon achievement of certain development, regulatory and commercialization milestones, for a potential total of up to $127 million. Enodia has also agreed to pay tiered royalties on net sales.

"Kezar has made significant early advances in the Sec61 field with the discovery of small molecule inhibitors," said Yves Ribeill, Chief Executive Officer of Enodia Therapeutics. "By integrating Kezar’s extensive preclinical datasets into our selective targeted protein degradation platform, this acquisition enhances our ability to make accelerated, yet informed development decisions across our candidate programs."

Enodia’s proprietary platform enables selective Sec61 Translocon modulation, a novel approach to inhibit disease-relevant proteins at the point of their synthesis before pathological effects occur, while preserving essential physiological functions. Enodia has built a broad and well-characterized chemical space spanning multiple Sec61 inhibitor families, supported by extensive biological datasets, including proteomics, Cryo-EM and tailored cell line libraries to enable rational small-molecule drug design powered by machine learning. Insights from Kezar’s Sec61-based programs will further strengthen Enodia’s core focus on Sec61-driven selectivity for targeting protein degradation.

"Kezar has spent nearly ten years pioneering research and drug discovery efforts around the Sec61 translocon and continues to have strong conviction in this novel target," said Chris Kirk, PhD, CEO of Kezar Life Sciences. "The team at Enodia is poised to make great progress in this space, and we are excited to see our efforts being carried on and expanded upon."

(Press release, Enodia Therapeutics, MAR 12, 2026, View Source [SID1234663500])

On March 12, 2026 PRISM BioLab Co., Ltd. ("PRISM") and Receptor.AI Inc. reported that they have entered into a drug discovery collaboration agreement (the "Collaboration") to develop an integrated, AI-navigated, physics-guided platform for the discovery of orally available small molecules targeting intracellular protein–protein interactions (PPIs), membrane proteins, and complex receptor systems.

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The Collaboration unites PRISM’s PepMetics chemistry — conformationally rigid, three-dimensional small molecules engineered to mimic α-helix and β-turn motifs — with Receptor.AI’s physics-informed, multi-objective AI navigation engine. By integrating their technologies, the companies aim to generate innovative hit, lead and clinical candidate compounds against PPI and membrane-protein targets that have proven challenging for conventional small molecule drug discovery, with an initial focus on metabolic diseases, including obesity.

The Collaboration will initially focus on one selected receptor target for metabolic disease. Receptor.AI will carry out molecular design using the combination of PRISM’s chemical space and Receptor.AI’s design algorithms. In parallel, the companies will jointly engage pharmaceutical partners interested in utilizing the combined capabilities of both technologies.

The Collaboration aims not only to generate clinical candidates—typically the goal of joint research — but also to showcase the power of combined technologies and to acquire specialized know‑how, which will be the basis for proposals to potential partner companies, enabling the expansion of future collaborative opportunities.

"We are very pleased to partner with Receptor.AI on this exciting project," said Dai Takehara, President & CEO of PRISM BioLab. "We have developed PepMetics Technology, a highly effective drug discovery platform targeting PPIs, and possess a unique peptide‑mimetic small‑molecule library, the PepMetics Library. We believe this library can be applied not only for intracellular PPI drug discovery but also for membrane proteins, which are not easily targeted by small molecules. With Receptor.AI’s AI‑based molecular design technologies ranging from peptides to small molecules, we expect the potential of the PepMetics Library to expand even further."

"We’re excited to partner with PRISM BioLab to move intracellular and receptor-driven discovery from ‘screening harder’ to navigating smarter," said Dr. Alan Nafiiev, Founder & CEO of Receptor.AI. "PRISM contributes a high-quality, structurally constrained virtual chemical space designed for practical progression. We’re bringing QuorumMap — our chemical space navigation engine — together with structure- and physics-informed modeling and multi-objective optimization to continuously reallocate compute and experimental focus toward the compounds most likely to translate: not just binders, but candidates that balance selectivity with the permeability and stability needed for oral exposure. The goal is a repeatable, decision-driven loop that turns difficult intracellular biology into actionable chemical hypotheses and ranked molecules ready for synthesis and testing."

PRISM and Receptor.AI share a common philosophy of "pursuing new approaches to drug discovery"—creating innovative therapeutics more rapidly, rationally, and with scientific rigor. Through this Collaboration, the companies aim to create synergies by mutually adopting state‑of‑the‑art drug discovery methods.

(Press release, PRISM BioLab, MAR 12, 2026, View Source [SID1234663519])

On March 11, 2026 CNS Pharmaceuticals presented its corporate presentation.

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(Presentation, CNS Pharmaceuticals, MAR 11, 2026, View Source [SID1234663453])

On March 11, 2026 CRISPR Therapeutics AG (Nasdaq: CRSP) (the "Company") reported the pricing of $550 million aggregate principal amount of its convertible senior notes due 2031 (the "notes") in a private offering (the "offering") to persons reasonably believed to be qualified institutional buyers pursuant to Rule 144A under the Securities Act of 1933, as amended (the "Securities Act"). The Company also granted the initial purchasers of the notes an option to purchase, for settlement within a period of 13 days from, and including, the date the notes are first issued, up to an additional $50 million aggregate principal amount of the notes. The sale of the notes is expected to close on March 16, 2026, subject to the satisfaction of customary closing conditions. The offering was upsized from the previously announced offering of $350 million aggregate principal amount of notes.

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The notes will be senior, unsecured obligations of the Company. The investors in the notes agreed to an effective coupon of 1.125%. Because of anticipated 35% withholding on interest payments on the notes under Swiss tax law, the Company agreed to increase the coupon by 0.6058% to 1.7308% to effectively eliminate the impact of such anticipated withholding on any noteholders who are not eligible to receive a refund. Interest will be payable semiannually in arrears on March 1 and September 1 of each year, beginning on September 1, 2026. The notes will mature on March 1, 2031, unless earlier converted, redeemed or repurchased.

Holders may convert all or any portion of their notes at their option at any time prior to the close of business on the business day immediately preceding the maturity date, other than during a "conversion freeze period" (as defined in the indenture that will govern the notes). Upon conversion, the Company will deliver for each $1,000 principal amount of converted notes a number of its common shares, nominal value CHF 0.03 per share ("common shares"), equal to the conversion rate.

The conversion rate will initially be 13.0617 common shares per $1,000 principal amount of notes (equivalent to an initial conversion price of approximately $76.56 per common share). The initial conversion price represents a premium of approximately 45% above the last reported sale price of $52.80 per common share on the Nasdaq Global Market on March 10, 2026. The conversion rate will be subject to adjustment in some events but will not be adjusted for any accrued and unpaid interest. In addition, if certain corporate events occur or are anticipated to occur prior to the maturity date or if the Company delivers a notice of optional redemption, the Company will, in certain circumstances, increase the conversion rate for a holder who elects to convert its notes in connection with such a corporate event or convert its notes called (or deemed called) for redemption in connection with such notice of optional redemption, as the case may be.

The Company may not redeem the notes prior to March 6, 2029. The Company may redeem for cash all or any portion of the notes (subject to certain limitations), at its option, on an optional redemption date occurring on or after March 6, 2029 if the last reported sale price of the common shares has been at least 130% of the conversion price for the notes then in effect for at least 20 trading days (whether or not consecutive) during any 30 consecutive trading day period (including the last trading day of such period) ending on, and including, the trading day immediately preceding the date on which the Company provides notice of optional redemption at a redemption price equal to 100% of the principal amount of the notes to be redeemed, plus accrued and unpaid interest to, but excluding, the optional redemption date. No sinking fund is provided for the notes.

If the Company undergoes a "fundamental change" (as defined in the indenture that will govern the notes), then, subject to certain conditions and limited exceptions, holders may require the Company to repurchase for cash all or any portion of their notes at a fundamental change repurchase price equal to 100% of the principal amount of the notes to be repurchased, plus accrued and unpaid interest to, but excluding, the fundamental change repurchase date.

The Company estimates that the net proceeds from the offering will be approximately $536.3 million (or approximately $585.2 million if the initial purchasers exercise their option to purchase additional notes in full), after deducting the initial purchasers’ discounts and commissions and estimated offering expenses payable by the Company. The Company intends to use the net proceeds from the offering for general corporate purposes.

The offer and sale of the notes and the common shares deliverable upon conversion of the notes have not been, and will not be, registered under the Securities Act or any other securities laws, and the notes and such shares cannot be offered or sold except pursuant to an exemption from, or in a transaction not subject to, the registration requirements of the Securities Act and any other applicable securities laws. This press release does not constitute an offer to sell, or the solicitation of an offer to buy, the notes or the common shares deliverable upon conversion of the notes, nor will there be any sale of the notes or such shares, in any state or other jurisdiction in which such offer, sale or solicitation would be unlawful.

(Press release, CRISPR Therapeutics, MAR 11, 2026, View Source [SID1234663454])

On March 11, 2026 Foghorn Therapeutics Inc. (Nasdaq: FHTX), a clinical-stage biotechnology company pioneering a new class of medicines that treat serious diseases by correcting abnormal gene expression, reported a financial and corporate update in conjunction with the Company’s 10-K filing for the year ending December 31, 2025. With an initial focus in oncology, Foghorn’s Gene Traffic Control Platform and resulting broad pipeline have the potential to transform the lives of people suffering from a wide spectrum of diseases.

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"We are building meaningful momentum as we further advance our first-in-class portfolio of potential medicines targeting cancers with significant unmet needs," said Adrian Gottschalk, President and Chief Executive Officer of Foghorn. "Our lead candidate FHD-909 continues to progress as planned through dose escalation in collaboration with Lilly. The trial is enriching for NSCLC patients with SMARCA4 mutations, where outcomes remain especially poor and deteriorate with later lines of therapy. In parallel, our wholly owned programs are moving toward the clinic. Our Selective CBP degrader program and our Selective EP300 degrader are on track for IND-enabling studies in 2026. Our recent cash infusion strengthens our balance sheet and enables us to focus on continued execution beyond our near-term milestones."

Recent Corporate Updates

Bolstered Balance Sheet. Announced the successful closing of a $50 million registered direct financing at $6.71 (issue price), a 30% premium to the closing price on January 9, 2026. The offering also included series warrants representing 50% coverage at $13.42 per share (two times the issue price) and another 50% coverage at $20.13 per share (three times the issue price). The transaction, supported by BVF Partners, Deerfield Management, founding investor Flagship Pioneering and a leading biotech mutual fund, strengthens the Company’s balance sheet and extends the anticipated cash runway into the first half of 2028.

Strengthened Executive Leadership. In February 2026, Foghorn appointed Ryan Maynard as Chief Financial Officer. Mr. Maynard joins Foghorn with over 25 years of executive experience driving financial strategy, capital markets execution, and operational performance across public and private biopharmaceutical companies.

Program Overview and Upcoming Milestones

FHD-909 (LY4050784). FHD-909 is a first-in-class oral SMARCA2 selective inhibitor that has demonstrated in preclinical studies to have high selectivity over its closely related paralog SMARCA4, two proteins that are the catalytic engines across all forms of the BAF complex. Selectively blocking SMARCA2 activity is a promising synthetic lethal strategy intended to induce tumor death while sparing healthy cells. SMARCA4 is mutated in up to 10% of NSCLC alone and implicated in a significant number of solid tumors. Across lines of therapy, significant unmet needs remain for patients with SMARCA4 (BRG1)-mutant cancers, with both poor response rates and short progression-free survival.
•Phase 1 trial on track. Enrollment in the first-in-human Phase 1 multi-center trial of FHD-909 is progressing well. The trial is on track, following the dosing of the first patient in October 2024.
•Synergistic preclinical data of FHD-909 in combination with pembrolizumab and KRAS inhibitors. Preclinical data support enhanced anti-tumor activity of FHD-909 in combination with standard-of-care (SoC) chemotherapies, anti-PD-1 pembrolizumab and several novel KRAS inhibitors in NSCLC animal models.
◦Pending successful Phase 1 dose escalation results, Foghorn and Lilly anticipate evaluating FHD-909 in combination studies in the front-line setting of NSCLC.

Ongoing strategic collaboration with Lilly. Foghorn is collaborating with Lilly to develop novel oncology medicines, including a 50/50 U.S. co-development and co-commercialization agreement for its selective SMARCA2 oncology program that includes both a selective inhibitor and a selective degrader, as well as an additional undisclosed oncology target. The collaboration also includes three discovery programs from Foghorn’s proprietary Gene Traffic Control platform.

Selective CBP degrader program. Foghorn’s Selective CBP degrader selectively targets CBP, an acetyltransferase closely related to EP300. CBP lineage dependencies are established in several cancers, including breast cancer, and there is also a synthetic relationship in EP300-mutated cancers, which include endometrial, cervical, ovarian, bladder, and colorectal cancer. Attempts to selectively drug CBP have been challenging due to the high level of similarity between the two proteins, while dual inhibition of CBP/EP300 has been associated with dose-limiting toxicities.

•Preclinical data for the Selective CBP degrader program identified CBPd-171 as a highly potent and selective lead candidate, which is currently advancing through dose-range finding toxicology studies.
•CBPd-171 demonstrates promising efficacy in ER+ breast cancer, while showing no impact on platelet counts and sparing megakaryocytes. Additionally, it demonstrates robust anti-tumor activity in EP300-mutant solid tumors and broader CBP-dependent cancers.
•A long-acting injectable (LAI) formulation has been optimized for subcutaneous administration on a weekly or every-other-week schedule, supporting convenient and patient-friendly dosing.
•Investigational New Drug (IND)-enabling studies anticipated in 2026.
Selective EP300 degrader program. Foghorn is developing a Selective EP300 degrader for the treatment of hematological malignancies and prostate cancer. Attempts to selectively drug EP300 have been challenging due to the high level of similarity between EP300 and CBP, while dual inhibition of CBP/EP300 has been associated with dose-limiting toxicities. EP300 lineage dependencies are established in several hematologic malignancies, which include diffuse large b-cell lymphoma (DLBCL) and multiple myeloma (MM).
•Preclinical efficacy and safety data for selective EP300 degraders in models of hematological malignancies demonstrate broad anti-tumor activity across more than 70% of hematologic sub-lineages tested, highlighting the program’s wide therapeutic potential.
•A VHL-based selective degrader has shown impressive efficacy in MM without hematologic toxicities, including thrombocytopenia, and EP300 degraders have retained full efficacy in IMiD-resistant multiple myeloma cell lines. Together, these findings support a favorable tolerability profile and suggest broad applicability in combination regimens across hematologic cancers.
•IND-enabling studies anticipated in 2026.
Selective ARID1B degrader program. Foghorn’s first-in-class Selective ARID1B degrader selectively targets and degrades ARID1B in ARID1A-mutated cancers. ARID1A is the most mutated subunit in the BAF complex and amongst the most mutated proteins in cancer. These mutations lead to a dependency on ARID1B in several types of cancer, including endometrial, gastric, gastroesophageal junction, bladder and NSCLC. Attempts to selectively drug ARID1B have been challenging because of the high degree of similarity between ARID1A and ARID1B and the fact that ARID1B has no enzymatic activity to target. ARID1B is a major synthetic lethal target implicated in up to 5% of all solid tumors.
•The preclinical program has made meaningful progress with the development of both VHL- and cereblon-based bifunctional degraders designed with potential for oral delivery. Both have achieved selective degradation of ARID1B, confirming effective target engagement, and have demonstrated modulation of downstream target genes consistent with ARID1B pathway disruption.
•Advancing towards in vivo proof of concept in 2026.

Chromatin Biology and Degrader Platform. Foghorn continues to advance its chromatin biology and degrader platform with investments in induced proximity, long-acting injectables, novel ligases, and oral delivery.

Full Year 2025 Financial Highlights

•Collaboration Revenues. Collaboration revenues were $30.9 million for the year ended December 31, 2025, compared to $22.6 million for the year ended December 31, 2024. The increase year-over-year was primarily driven by continued advancement of programs under the Lilly Collaboration Agreement.

•Research and Development Expenses. Research and development expenses were $85.5 million for the year ended December 31, 2025, compared to $94.5 million for the year ended December 31, 2024. This decrease was primarily due to a decrease in FHD-286 costs, decreases in personnel-related costs, early development and other research external costs and facilities and IT-related expenses, partially offset by an increase in Lilly-partnered programs.

•General and Administrative Expenses. General and administrative expenses were $27.6 million for the year ended December 31, 2025, compared to $28.4 million for the year ended December 31, 2024. This decrease was primarily due to lower facilities and IT related expenses.

•Net Loss. Net loss was $74.3 million for the year ended December 31, 2025, compared to a net loss of $86.6 million for the year ended December 31, 2024.

•Cash, Cash Equivalents and Marketable Securities. As of December 31, 2025, the Company had $158.9 million in cash, cash equivalents and marketable securities, providing cash runway into the first half of 2028.

About FHD-909
FHD-909 (LY4050784) is a potent, first-in-class, allosteric, and orally available small molecule that selectively inhibits the ATPase activity of SMARCA2 (BRM) over its closely related paralog SMARCA4 (BRG1), two proteins that are the catalytic engines across all forms of the BAF complex, one of the key regulators of the chromatin regulatory system. In preclinical studies, tumors with mutations in SMARCA4 rely on SMARCA2 for their survival. FHD-909 has shown significant anti-tumor activity across multiple SMARCA4-mutant lung tumor models.

(Press release, Foghorn Therapeutics, MAR 11, 2026, View Source [SID1234663455])