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 12, 2026 Atara Biotherapeutics, Inc. (Nasdaq: ATRA), a leader in T-cell immunotherapy, leveraging its novel allogeneic Epstein-Barr virus (EBV) T-cell platform to develop transformative therapies for patients with cancer and autoimmune diseases, reported that a Type A meeting with the U.S. Food and Drug Administration (FDA) has been scheduled to discuss the Complete Response Letter (CRL) to the Biologics License Application (BLA) for tabelecleucel (tab-cel) held by our partner Pierre Fabre Pharmaceuticals.

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Pierre Fabre Pharmaceuticals, with Atara’s support, will meet with the agency to collaboratively address the points from the CRL and enable a resubmission with the additional efficacy data that has been collected since the original BLA submission.

"We are pleased that the FDA has granted a Type A Meeting to our partner, Pierre Fabre, and hope to gain clarity on a path forward for re-submission of the tab-cel BLA," said Cokey Nguyen, President and Chief Executive Officer of Atara. "We anticipate providing a regulatory update in the second quarter."

(Press release, Atara Biotherapeutics, MAR 12, 2026, View Source [SID1234663486])

On March 12, 2026 Lyell Immunopharma, Inc. (Nasdaq: LYEL), a late-stage clinical company advancing a pipeline of next-generation chimeric antigen receptor (CAR) T-cell therapies for patients with cancer, reported financial results and business highlights for the fourth quarter and year ended December 31, 2025. Lyell has since commenced patient dosing in the first-of-its-kind Phase 3 head-to-head CAR T-cell randomized controlled clinical trial of rondecabtagene autoleucel (ronde-cel) versus investigator’s choice of axicabtagene ciloleucel (axi-cel) or lisocabtagene maraleucel (liso-cel) in patients with relapsed/refractory (R/R) large B-cell lymphoma (LBCL) with disease progression on at least one prior line of therapy (PiNACLE-H2H). Lyell has dosed seven new patients with metastatic colorectal cancer (mCRC) with LYL273, an enhanced guanylyl cyclase C (GCC)-targeted CAR T-cell product candidate, since its November 2025 acquisition, without dose-limiting toxicity and including dose escalation to Dose Level 3.

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Lyell also recently announced it has closed the sale of an additional $50 million of shares of its common stock to investors from its July 2025 equity private placement of up to $100 million, following achievement of a clinical milestone within its PiNACLE pivotal trial evaluating ronde-cel in patients with R/R LBCL in the third- or later-line setting (3L+), and the appointment of Smital Shah as its Chief Financial and Business Officer.

"Lyell is on track to achieve multiple clinical milestones in the next 12 to 18 months. We have now advanced ronde-cel into two pivotal clinical trials, with the pivotal data supporting BLA submission from the PiNACLE trial expected to be reported mid-next year," said Lynn Seely, M.D., President and Chief Executive Officer of Lyell. "With the encouraging emerging safety profile and clinical activity observed with LYL273 in patients with metastatic colorectal cancer, we believe Lyell is well-positioned with two next-generation CAR T‑cell product candidates."

Fourth Quarter Updates and Recent Business Highlights

Ronde-cel: A next-generation dual-targeting CD19/CD20 CAR T-cell product candidate designed to increase complete response rates and prolong the duration of response as compared to approved CD19‑targeted CAR T-cell therapies for the treatment of LBCL

Ronde-cel is an autologous CAR T-cell product candidate with a true ‘OR’ logic gate to target B cells that express either CD19 or CD20 with full potency and is manufactured with a process that enriches for CD62L-positive cells to generate more naïve and central memory CAR T cells with enhanced stemlike features and antitumor activity. Ronde-cel has received from the U.S. Food and Drug Administration (FDA) Regenerative Medicine Advanced Therapy (RMAT) designation as well as Fast Track designation for the treatment of adults with R/R LBCL.

•The pivotal PiNACLE single-arm trial is a seamless expansion of the 3L+ cohort in the Phase 1/2 multi-cohort trial and is evaluating ronde-cel at a dose of 100 x 106 CAR T cells in patients with R/R LBCL. The trial is expected to enroll approximately 120 patients in the inpatient or outpatient setting, and there is no upper age limit for eligibility. The primary endpoint of the trial is the overall response rate, including an evaluation of duration of response.

•Patient dosing commenced in February 2026 in PiNACLE-H2H, the Phase 3 randomized controlled trial evaluating ronde-cel versus investigator’s choice of axi-cel or liso-cel in patients with R/R LBCL in the 2L setting. The trial is expected to enroll approximately 400 patients (200 per arm) at sites in the US, Canada and Australia. Patients may be treated in either the inpatient or outpatient setting. The trial’s primary endpoint is event-free survival.
•Updated data from the ongoing Phase 1/2 clinical trial were presented at the December 2025 American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition (ASH 2025):
◦A best overall response rate of 93% and a complete response rate of 76% in 29 efficacy-evaluable patients with R/R LBCL in the 3L+ setting. The median progression-free survival was 18 months as of the data cutoff date of September 5, 2025.
◦Data were also presented from the 2L cohort in the Phase 1/2 multi-cohort clinical trial, including an efficacy-evaluable population of 18 patients (94% with high-risk primary refractory disease) and demonstrated an 83% best overall response rate and a 61% complete response rate.
◦The safety profile was appropriate for outpatient administration. Data from 25 patients treated with ronde-cel who received dexamethasone prophylaxis in the 3L+ and 2L settings revealed no events of ≥ Grade 3 cytokine release syndrome and a 4% rate of ≥ Grade 3 immune cell-associated neurotoxicity syndrome.
LYL273 (formerly known as GCC19CART): A next-generation GCC-targeted CAR T-cell product candidate for the treatment of mCRC and other GCC-expressing cancers
LYL273 is a GCC-targeted CAR T-cell product candidate enhanced with CD19 CAR expression and controlled cytokine release, designed to improve CAR T-cell expansion, immune cell infiltration and cancer cell killing in the hostile tumor microenvironment. In November 2025, we acquired global rights (excluding mainland China, Hong Kong, Macau and Taiwan) to LYL273, which has shown promising dose-dependent clinical activity in patients with advanced mCRC in a Phase 1 trial conducted in the U.S. LYL273 received from the FDA Fast Track designation for the treatment of mCRC.
•The U.S. Phase 1 clinical trial is continuing to enroll patients to determine the recommended Phase 2 dose. Seven additional patients with mCRC have been treated with LYL273 since the November 2025 acquisition without dose-limiting toxicity and including dose escalation to Dose Level 3.

•A 67% best overall response rate, an 83% disease control rate and an 8-month median progression-free survival with a manageable safety profile have been reported at the highest dose level tested as of the data cutoff date of October 28, 2025 (Dose Level 2) in patients with refractory mCRC in the U.S. Phase 1 clinical trial.

Fourth Quarter and Full Year 2025 Financial Results

Lyell reported a net loss of $140.7 million and $274.4 million for the fourth quarter and year ended December 31, 2025, respectively, compared to a net loss of $191.9 million and $343.0 million for the same periods in 2024. Net loss for the fourth quarter and year ended December 31, 2025 included $66.3 million in acquired in-process research and development (IPR&D) expense as part of the acquisition of our rights to LYL273, and $19.7 million in stock-based compensation expense for an equity milestone deemed probable related to the LYL273 license acquisition. Net loss for the fourth quarter and year ended December 31, 2024 included $87.2 million in acquired IPR&D expense as part of our acquisition of ImmPACT Bio and $51.3 million of long‑lived asset impairment expense. Non‑GAAP net loss, which excludes stock-based compensation, non-cash expenses related to the change in the estimated fair value of success payment liabilities and securities purchase agreement put/call liability, long‑lived asset impairment expense and certain non-cash investment gains and charges, was $33.1 million and $144.8 million for the fourth quarter and year ended December 31, 2025, respectively, compared to $45.9 million and $159.5 million for the same periods in 2024.

GAAP and Non-GAAP Operating Expenses

•Research and development (R&D) expenses were $52.2 million for the fourth quarter ended December 31, 2025, compared to $48.7 million for the same period in 2024. The increase in fourth quarter 2025 R&D expenses of $3.5 million was primarily due to $19.7 million in stock-based compensation expense for an equity milestone deemed probable related to the LYL273 license acquisition. The increase in fourth quarter 2025 R&D expenses was partially offset by an $8.9 million reduction in personnel costs and a $4.7 million reduction in additional facilities and technology costs primarily due to reduced headcount following the successful technology transfer of ronde-cel to our LyFE Manufacturing CenterTM (LyFE) and associated workforce reduction in the first half of 2025. Non‑GAAP R&D expenses, which exclude non-cash stock-based compensation and non-cash expenses related to the change in the estimated fair value of success payment liabilities for the fourth quarter ended December 31, 2025, were $30.1 million compared to $45.4 million for the same period in 2024 due to the workforce reduction related to the successful technology transfer of ronde-cel.
•General and administrative (G&A) expenses were $10.6 million for the fourth quarter ended December 31, 2025, compared to $14.5 million for the same period in 2024. The decrease in fourth quarter 2025 G&A expenses of $3.9 million was primarily due to a $4.1 million decrease in personnel costs associated with the workforce reduction related to the successful ronde-cel technology transfer, partially offset by a $0.8 million increase in collaborations and licenses expenses.
A discussion of non-GAAP financial measures, including reconciliations of the most comparable U.S. generally accepted accounting principles (GAAP) measures to non‑GAAP financial measures, is presented below under "Non-GAAP Financial Measures."
Cash, cash equivalents and marketable securities
Cash, cash equivalents and marketable securities as of December 31, 2025 were approximately $247.2 million (excluding the $50 million tranche received in March 2026), compared to approximately $383.5 million as of December 31, 2024. Lyell believes that its current cash, cash equivalents and marketable securities balances will be sufficient to meet working capital and capital expenditure needs into the second quarter of 2027.

(Press release, Lyell Immunopharma, MAR 12, 2026, View Source [SID1234663501])

On March 12, 2026 Pilatus Biosciences, Inc., a clinical-stage biopharmaceutical company developing novel metabolic checkpoint immunotherapies for liver and gastrointestinal cancers, reported the first patient has been dosed in its Phase 1 clinical trial evaluating PLT012, a first-in-class anti-CD36 monoclonal antibody for the treatment of advanced solid tumors. The first patient was treated at Next Oncology in Houston, Texas.

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PLT012 recently received Investigational New Drug (IND) clearance from the U.S. Food and Drug Administration. The antibody target, CD36, is a key regulator of lipid uptake and metabolic adaptation within the tumor microenvironment (TME). By blocking CD36-mediated fatty acid uptake, PLT012 aims to invigorate innate and adaptive effector cells, reduce immunosuppressive cell populations, and elicit durable tumoricidal immune responses.

"Dosing our first patient is an important milestone for Pilatus and validates our work advancing a new immuno-metabolic approach to cancer therapy," said Raven Lin, CEO and Co-Founder, Pilatus Biosciences. "Many solid tumors create a metabolically hostile microenvironment that drives immune exhaustion and resistance to existing therapies. PLT012 is designed to directly address this metabolic suppression, with the goal of restoring effective antitumor immunity for patients with limited treatment options."

"Many advanced solid tumors suppress immune responses through metabolic mechanisms, limiting the effectiveness of current immunotherapies," said Anthony B. El-Khoueiry, MD, principal investigator of the trial, who also serves as chief of section of developmental therapeutics and associate director for clinical research at the USC Norris Comprehensive Cancer Center, part of Keck Medicine of USC. "CD36 is a key regulator of lipid uptake and immune dysfunction in the tumor microenvironment, making it a compelling target. This Phase 1 study will evaluate the safety of PLT012 and help determine whether targeting metabolic checkpoints can restore immune activity for patients with difficult-to-treat cancers."

The open-label, multi-center Phase 1 study is evaluating PLT012 in patients with advanced solid tumors, with expansion cohorts planned in tumor types characterized by lipid-driven metabolic dysregulation, including, but not limited to, liver cancers and tumors with liver metastases. The primary objectives of the study are to assess safety and tolerability, and to determine the maximum tolerated dose and the recommended Phase 2 dose of PLT012.

Additional endpoints will look at pharmacokinetics/pharmacodynamics, biomarkers, and early signs of clinical response. In addition to pharmacokinetics and immunogenicity, a comprehensive biomarker strategy centered on CD36 biology has been designed to support translational insights and guide future clinical development. This approach is intended to enable more precise patient stratification in expansion cohorts and subsequent trials, with the goal of enriching for lipid-enriched tumor types and CD36-high patient populations.

"There is a significant unmet need for patients whose tumors do not respond adequately to current immunotherapies," said George E. Peoples, MD, Chief Medical Officer, Pilatus Biosciences. "Targeting CD36 represents a differentiated approach to reshape the tumor microenvironment by addressing lipid-driven immune dysfunction. The comprehensive clinical and biomarker assessments incorporated into this study will be essential to understanding how PLT012 reprograms the TME and to guiding further development."

Preclinical studies demonstrated that PLT012 blocked CD36-mediated metabolic reprogramming in regulatory T cells (Tregs) and CD8+ tumor-infiltrating lymphocytes, resulting in enhanced antitumor immune activity. In murine models of liver metastasis, PLT012 significantly reduced tumor growth in both hepatic and subcutaneous tumors. These effects were associated with favorable remodeling of the TME, including reduced M2 macrophages and Treg populations, and increased CD8+ T cell infiltration.

Additionally, PLT012 mitigated liver metastasis–associated resistance to immune checkpoint inhibitors and resensitized tumors to anti-PD-1 therapy in preclinical models. Together, these findings support the potential of CD36-targeted immunometabolic therapy as a complementary strategy to existing checkpoint blockade treatments.

Building on previously reported preclinical data demonstrating PLT012’s robust anti-tumor activity in both inflamed and immune-cold HCC murine models, PLT012 received Orphan Drug Designation from the FDA in December 2024 for the treatment of hepatocellular carcinoma (HCC) and intrahepatic bile duct cancers, underscoring the significant unmet medical need in these indications. Pilatus also received FDA Fast Track Designation for PLT012 for the treatment of HCC on February 14, 2026.

This announcement is intended to share information about this study and is not soliciting participants.

About PLT012

PLT012 is a humanized monoclonal antibody designed to selectively block CD36-mediated lipid uptake, a key mechanism driving immunosuppression and immune exclusion within the tumor microenvironment. By targeting lipid metabolism, PLT012 exerts a unique mechanism of action: it depletes immunosuppressive cell populations, including Tregs and pro-tumor macrophages, while simultaneously enhancing antitumor activities of intratumoral NK cell and cytotoxic CD8+ T cell that are otherwise susceptible to lipid-induced exhaustion. In preclinical studies, PLT012 has demonstrated potent monotherapy efficacy in models of liver malignancies, with a favorable safety profile across species. Leveraging its distinct mechanism of action, PLT012 further acts as a potent sensitizer in combination with anti–PD-L1 therapies, effectively overcoming drug resistance in immune "cold" tumors and liver metastases.

(Press release, Pilatus Biosciences, MAR 12, 2026, View Source [SID1234663520])

On March 12, 2026 Bolt Biotherapeutics (Nasdaq: BOLT), a clinical-stage biopharmaceutical company developing novel immunotherapies for the treatment of cancer, reported financial results for the fourth quarter and full-year ended December 31, 2025, and provided a business update.

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"BDC‑4182 is the first of our next‑generation Boltbody ISACs to enter the clinic, and we saw a clear difference versus our first-gen ISACs in terms of immune response from the very first patient treated," said Willie Quinn, President and Chief Executive Officer. "The ISAC mechanism is radically different from ADCs and T cell engagers, and we believe that demonstrating anti-tumor activity with BDC-4182 will unlock an entirely new approach to treating cancer. We continue to enroll patients with gastric and gastroesophageal cancers in the Phase 1 dose‑escalation trial and remain on track to report initial data in the third quarter of 2026."

Recent Highlights and Anticipated Milestones

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Initial clinical data from BDC-4182 Phase 1 study for patients with gastric and gastroesophageal cancer expected in the third quarter of 2026. BDC-4182 is a next-generation BoltbodyTM ISAC targeting claudin 18.2, a clinically validated target with expression in gastric cancer, gastroesophageal junction cancer, pancreatic cancer, and other tumor types. In preclinical models, including cancer models with low claudin 18.2 expression, BDC-4182 demonstrated significant anti-tumor activity, induced immunological memory, and outperformed cytotoxic claudin 18.2 ADCs. Following a strong immune response that was observed at the initial dose levels, Bolt modified the clinical trial protocol to allow for step-up dosing, which has been successfully used commercially for T-cell engagers. The clinical trial in gastric and gastroesophageal cancers is ongoing, and the Company expects to present initial clinical data in the third quarter of 2026.
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Next-generation Boltbody ISACs targeting CEA and PD-L1. Bolt has two ISAC programs in preclinical development. Both programs are on hold pending partnering or funding and have the potential to be in the clinic within 18 months once activities resume.
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Bolt’s CEA-targeted ISAC comprises a novel, fully human antibody with high affinity and selectivity to CEACAM5 (CEA), and not to other members of the CEACAM family, conjugated to a proprietary next-generation TLR7/8 agonist via a non-cleavable linker. Bolt’s CEA ISAC induced complete and durable anti-tumor responses in preclinical models and was more effective than a Topo1-based ADC at lower doses and in a lower antigen density tumor model. This CEA ISAC was well tolerated in a non-GLP toxicology study.

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Bolt’s PD-L1 ISAC utilizes a novel human anti-PD-L1 antibody conjugated to a TLR7/8 agonist via a non-cleavable linker. This ISAC leverages a unique mechanism of action due to its ability to target both tumor and immune cells that express PD-L1. Preclinical results demonstrated that PD-L1 ISACs represent a compelling new approach to treat cancer, leveraging mechanisms that are distinct from and potentially complementary to conventional PD-1/PD-L1 blockade with the potential for enhanced immune activation and antitumor activity.
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Cash, cash equivalents, and marketable securities were $31.8 million as of December 31, 2025. Cash on hand is expected to fund multiple milestones and operations into 2027.

Fourth Quarter and Full Year 2025 Financial Results

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Collaboration Revenue – Total collaboration revenue was $2.5 million and $7.7 million for the fourth quarter and full year ended December 31, 2025, respectively, compared to zero and $7.7 million for the same quarter and year in 2024, respectively. Revenue in the fourth quarter and full year ended 2025 was due to continued progress in our collaborations as we fulfill our performance obligations to our collaboration partners. We reported no collaboration revenue in the fourth quarter of 2024 as a result of the reassessment of our expected future performance obligations.

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Research and Development (R&D) Expenses – R&D expenses were $5.0 million for the fourth quarter and $28.5 million for the full year ended December 31, 2025, respectively, compared to $11.7 million and $57.5 million for the same quarter and year in 2024, respectively. The decrease between the comparable periods was mainly due to a continued decrease in salary and related expenses primarily as a result of our restructuring plans, reduced clinical trial expenses and lower research and development expenses.

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General and Administrative (G&A) Expenses – G&A expenses were $3.1 million for the fourth quarter and $13.8 million for the full year ended December 31, 2025, respectively, compared to $3.9 million and $18.5 million for the same quarter and year in 2024, respectively. The decrease between the comparable periods was mainly due to a continued decrease in salary and related expenses primarily as a result of our restructuring plans.

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Loss from Operations – Loss from operations was $7.1 million for the fourth quarter and $36.1 million for the full year ended December 31, 2025, respectively, compared to $16.9 million and $73.0 million for the same quarter and year in 2024, respectively.

About the Boltbody Immune-Stimulating Antibody Conjugate (ISAC) Platform
Bolt Biotherapeutics’ Boltbody ISAC platform harnesses the precision of antibodies with the power of the innate and adaptive immune system to generate a productive anti-cancer response. Each Boltbody ISAC candidate comprises a tumor-targeting antibody, a non-cleavable linker, and a proprietary immune stimulant. The antibody is designed to target one or more markers on the surface of a tumor cell and the immune stimulant is designed to recruit and activate myeloid cells. Activated myeloid cells initiate a positive feedback loop by releasing cytokines and chemokines, chemical signals that attract other immune cells and lower the activation threshold for an immune response. This increases the population of activated immune system cells in the tumor microenvironment and promotes a robust immune response with the goal of generating durable therapeutic responses for patients with cancer.

(Press release, Bolt Biotherapeutics, MAR 12, 2026, View Source [SID1234663487])