On May 12, 2026 MiNK Therapeutics, Inc. (NASDAQ: INKT), a clinical-stage biopharmaceutical company developing allogeneic invariant natural killer T (iNKT) cell therapies for cancer and immune disorders, reported data being presented at the American Society of Gene and Cell Therapy Annual Meeting (ASGCT 2026) in Boston, Massachusetts. The data demonstrate that agenT-797, MiNK’s off-the-shelf, allogeneic iNKT cell therapy produces fundamentally different, disease-appropriate immune responses in patients with solid tumors and patients with acute respiratory distress syndrome (ARDS), driven by the intrinsic biology of iNKT cells rather than genetic modification.

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The data, to be presented in Poster 3371 on May 14, 2026, by Dr. Yan demonstrates that the same agenT-797 product, manufactured from the same donor batch and administered without modification, drove a TH1 pro-inflammatory immune program in 34 patients with solid tumors and a TH2 anti-inflammatory immune response in 20 patients with ARDS. The findings were consistent across multiple manufacturing batches and donors, establishing platform reproducibility at scale.

"The same off-the-shelf cell — from the same donor, same manufacturing batch — drives inflammation in a tumor and restores immune homeostasis in a failing lung. Without modification. Without engineering. That is intrinsic iNKT biology, and it is the foundation of a scalable platform we believe is applicable across oncology, critical illness, and beyond. To our knowledge, no prior cellular therapy platform has demonstrated this type of disease-directed immune response across two fundamentally different diseases from a single manufacturing run," said, Jennifer Buell, Ph.D., President and Chief Executive Officer, MiNK Therapeutics.

These findings further support the scalability and consistency of MiNK’s proprietary manufacturing platform, which is designed to isolate donor-derived iNKT cells and reproducibly expand them to billions of cells per donor while preserving intrinsic biological activity across disease settings. agenT-797 is cryopreserved, HLA-independent, and requires no lymphodepletion, supporting potential use across acute critical care, oncology, and post-transplant immune dysfunction.

ASGCT Poster 3371: Context-Dependent Immune Reprogramming in Cancer and ARDS

Clinical evidence of effector function: agenT-797 was associated with tumor clearance and durable response in patients with cancer, including complete resolution of metastatic disease in germ cell testicular cancer treated with agenT-797 plus anti-PD-1 (Garmezy et al., Oncogene, 2025). In ARDS, agenT-797 was associated with improved survival and radiographic resolution of ARDS relative to in-hospital controls, including clearance of carbapenem-resistant Pseudomonas pneumonia in a 21-year-old patient on veno-venous ECMO.
In 34 solid tumor patients (NCT05108623), agenT-797 infusion produced rapid IFN-gamma elevation — a TH1 pro-inflammatory signature consistent with anti-tumor immune activation.
In 20 ARDS patients (NCT04582201), the same product from the same manufacturing donor batch produced IL-4 and IL-13 elevation — a TH2 anti-inflammatory signature consistent with immune restoration and lung injury recovery.
Favorable safety profile: Immune activation across both oncology and ARDS settings occurred without evidence of uncontrolled cytokine release syndrome or pathologic hyperinflammation, supporting a favorable therapeutic index appropriate for the ICU setting.

"What makes these findings compelling is that we are observing the same unmodified iNKT cell product generate fundamentally different immune responses across distinct disease states in a biologically coherent and clinically relevant manner," said Terese C. Hammond, MD, Head of Inflammatory and Pulmonary Diseases, MiNK Therapeutics. "These findings support the idea that iNKT cells function as coordinated immune effectors capable of dynamically modulating inflammatory and restorative pathways based on the disease environment. In critical illness, effective therapy may require coordinated immune activation, restoration, and pathogen-directed response occurring simultaneously. The Phase 1/2 clinical data suggested this biology was possible; the ASGCT (Free ASGCT Whitepaper) findings now provide mechanistic evidence supporting how agenT-797 may achieve those effects."

(Press release, MiNK Therapeutics, MAY 12, 2026, View Source [SID1234665582])

On May 12, 2026 Caribou Biosciences, Inc. (Nasdaq: CRBU), a leading clinical-stage CRISPR genome-editing biopharmaceutical company, reported two abstracts have been accepted for oral presentations at the 2026 European Hematology Association (EHA) (Free EHA Whitepaper) Annual Meeting, which will be held June 11-14, 2026, in Stockholm, Sweden.

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The first oral presentation will highlight the long-term durability of a single dose of vispa-cel in patients enrolled in the ANTLER phase 1 clinical trial for relapsed or refractory B cell non-Hodgkin lymphoma. Details of the ANTLER phase 1 presentation are as follows:

Title: Vispa-cel, an allogeneic anti-CD19 CAR-T cell therapy with a PD-1 knockout, in patients with relapsed/refractory B cell non-Hodgkin lymphoma (ANTLER phase 1 clinical trial)
Presenter: Stephen J. Schuster, MD, Robert and Margarita Louis-Dreyfus professor of chronic lymphocytic leukemia and lymphoma; department of medicine, hematology-oncology division;
director, lymphoma program and lymphoma translational research; Abramson Cancer Center, University of Pennsylvania
Date and time: Friday, June 12, 2026, at 5:15 – 6:30pm CEST
Session: Prospective lymphoma trials
Location: Nobel Hall
Abstract number: S236

The second oral presentation includes longer follow-up from patients enrolled in the dose escalation portion of the ongoing CaMMouflage phase 1 clinical trial evaluating CB-011 in patients with relapsed or refractory multiple myeloma. Details of the CaMMouflage phase 1 presentation are as follows:

Title: CB-011, an allogeneic anti-BCMA CAR-T cell therapy with immune cloaking, for patients with relapsed/refractory multiple myeloma (CaMMouflage phase 1 trial)
Presenter: Binod Dhakal, MD, associate professor of medicine, Medical College of Wisconsin
Date and time: Sunday, June 14, 2026, at 11:00am – 12:15pm CEST
Session: Immunotherapy in multiple myeloma
Location: Victoria Hall
Abstract number: S201

Accepted abstracts are now available on the EHA (Free EHA Whitepaper) Annual Meeting website.

About vispacabtagene regedleucel
Vispacabtagene regedleucel (vispa-cel; formerly known as CB-010) is an allogeneic anti-CD19 CAR-T cell therapy evaluated in patients with relapsed or refractory B cell non-Hodgkin lymphoma (r/r B-NHL). To Caribou’s knowledge, vispa-cel is the first allogeneic CAR-T cell therapy in the clinic with a PD-1 knockout, a genome-editing strategy designed to enhance CAR-T cell activity by limiting premature CAR-T cell exhaustion. The FDA granted vispa-cel Regenerative Medicine Advanced Therapy (RMAT), Fast Track, and Orphan Drug designations for B-NHL.

About the ANTLER phase 1 clinical trial
The ANTLER phase 1 clinical trial evaluated vispa-cel in adult patients with r/r B-NHL in a multicenter, open-label trial. As of a September 2, 2025, data cutoff date, 84 patients were treated in the trial. Using a 3+3 enrollment strategy, safety and efficacy were assessed in 16 patients in dose escalation who received a single dose of 40×106, 80×106, or 120×106 CAR-T cells preceded by a lymphodepletion (LD) regimen of cyclophosphamide at 60 mg/kg/day for 2 days followed by fludarabine at 25 mg/m2/day for 5 days. Eighty million (80×106) CAR-T cells was selected as the recommended phase 2 dose (RP2D). Sixty-three second-line large B cell lymphoma (2L LBCL) patients received a single dose of vispa-cel during dose expansion. Five patients were enrolled in a cohort of third-line or later LBCL patients with prior exposure to CD19-targeted therapy. Additional information on the ANTLER trial (NCT04637763) can be found at www.clinicaltrials.gov.

About CB-011
CB-011 is an allogeneic anti-BCMA CAR-T cell therapy being evaluated in patients with relapsed or refractory multiple myeloma (r/r MM). To Caribou’s knowledge, CB-011 is the first allogeneic CAR-T cell therapy in the clinic that is engineered to enable activity through an immune cloaking strategy with a B2M knockout and insertion of a B2M–HLA-E fusion protein to blunt immune-mediated rejection. The FDA granted CB-011 RMAT, Fast Track, and Orphan Drug designations for r/r MM.

About the CaMMouflage phase 1 clinical trial
The CaMMouflage clinical trial is a multicenter, open-label phase 1 trial evaluating CB-011 in adults with r/r MM who have been treated with three or more prior lines of therapy. Using a 3+3 dose escalation design, safety and efficacy of CB-011 were evaluated in 48 patients at multiple dose levels and two different lymphodepletion (LD) regimens. Thirteen patients were treated with a single dose of CB-011 (50×106 [N=3], 150×106 [N=7], and 450×106 [N=3] CAR-T cells) with an LD regimen of 300 mg/m2 cyclophosphamide and 30 mg/m2 fludarabine daily for 3 days, and 35 patients were treated with a single dose of CB-011 (150×106 [N=6], 300×106 [N=13], 450×106 [N=13], and 800×106 [N=3] CAR-T cells) with an LD regimen of 500 mg/m2 cyclophosphamide and 30 mg/m2 fludarabine daily for 3 days. The dose expansion portion of the trial is evaluating safety and efficacy of CB-011 at 450×106 CAR-T cells with the selected LD of 500 mg/m2 cyclophosphamide and 30 mg/m2 fludarabine daily for three days. Additional information on the CaMMouflage trial (NCT05722418) can be found at www.clinicaltrials.gov.

(Press release, Caribou Biosciences, MAY 12, 2026, View Source [SID1234665581])

On May 12, 2026 BlossomHill Therapeutics, Inc., a privately-held, clinical-stage biopharmaceutical company applying an intentional, chemistry-based approach to develop innovative small molecule medicines for the treatment of cancer, reported that initial dose escalation data from its Phase 1/1b trial of BH-30236, a macrocyclic CDC-link kinase (CLK) inhibitor, in relapsed or refractory acute myeloid leukemia (R/R AML) and higher-risk myelodysplastic syndrome (HR-MDS) will be presented during a poster session on June 12, 2026, at the European Hematology Association (EHA) (Free EHA Whitepaper) 2026 Congress in Stockholm, Sweden. Additionally, BH-30236 has been granted orphan drug designation by the U.S. Food and Drug Administration for the treatment of AML.

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"We are highly encouraged by the initial safety data and early signs of anti-leukemic activity observed with BH-30236, both as a monotherapy and in combination with venetoclax," said Jean Cui, Ph.D., Founder and Chief Executive Officer of BlossomHill Therapeutics. "By modulating aberrant alternative mRNA splicing, our potential first-in-class CLK inhibitor, BH-30236, represents a novel approach for patients with relapsed or refractory AML and higher-risk MDS, who face a significant unmet medical need. We look forward to presenting additional data from more patients with longer follow-up at the meeting and to advancing BH-30236 in both monotherapy and combination settings."

BH-30236 was designed to target the CLK kinase family, leading to the modulation of aberrant alternative mRNA splicing, a defining feature implicated in cancer progression and therapeutic resistance across both hematologic malignancies and solid tumors. Our Phase 1/1b trial evaluating BH-30236 was initiated following encouraging preclinical data, including evidence of synergistic activity between BH-30236 and venetoclax, a BCL-2 inhibitor and an established standard of care therapy for patients with AML. The trial is currently enrolling patients in dose escalation, evaluating BH-30236 as both a monotherapy and in combination with venetoclax.

As of the January 23, 2026 cutoff date for the EHA (Free EHA Whitepaper) abstract submission, 28 patients received BH-30236 monotherapy at 5-120 mg on a continuous daily administration schedule (QD) and 11 patients received BH-30236 at 20-60mg QD in combination with venetoclax. Initial findings demonstrated:

BH-30236 was generally well tolerated as both a monotherapy and in combination with venetoclax, with most treatment-related adverse events being low-grade and manageable, as well as one grade 3 DLT (diarrhea)
Dose escalation showed predictable pharmacokinetics without drug accumulation or reduction, and no significant drug-drug interactions were observed with venetoclax
Early signs of clinical activity were observed:
In the monotherapy cohort, 29% (n=5) of evaluable patients achieved at least a 50% reduction in bone marrow blast counts, including one HR-MDS patient treated at 60 mg with ongoing blast count reduction with duration of treatment 7.6 months.
In the combination cohort, 55% (n=5) of evaluable patients experienced at least a 50% blast reduction, including one patient refractory to all prior therapy including venetoclax, who achieved a minimal residual disease (MRD)-negative complete remission.
"In March of this year, the U.S. Food and Drug Administration granted Orphan Drug Designation to BH-30236 for the treatment of acute myeloid leukemia, underscoring the need for new therapies in this rare malignancy," said Dr. Geoff Oxnard, Chief Medical Officer of BlossomHill Therapeutics. "This designation is an important milestone that reflects the potential of BH-30236 to address a significant unmet need and provides benefits that may support our ongoing clinical development, as well as potential market exclusivity upon approval."

Poster Session Details

Title: A First-in-Human Study of the Oral CLK Inhibitor BH-30236 in Adults with Relapsed/Refractory Acute Myeloid Leukemia or Higer-Rish Myelodysplastic Syndrome: Monotherapy and Venetoclax Combination
Presenting Author: Eytan M. Stein, MD, Chief of the Leukemia Service, Associate Attending Physician, Clinical Investigator and Director of the Program for Drug Development in Leukemia on the Leukemia Service at Memorial Sloan Kettering Cancer Center
Date & Time: Friday, June 12 from 12:45 to 1:45 ET / 18:45 – 19:45 CEST
Abstract Code: PF494
About BH-30236
BH-30236 is an investigational orally bioavailable, macrocyclic inhibitor of the CDC-like kinase (CLK) family. BH-30236 is designed to modulate aberrant alternative splicing in cancerous tissue, targeting the same aberrant splicing machinery that drives acute myeloid leukemia (AML) and higher-risk myelodysplastic syndrome (HR-MDS) disease biology and that cancer cells exploit to develop resistance to venetoclax, FLT3 inhibitors and cytarabine. BH-30236 is currently in clinical development for the treatment of relapsed or refractory AML (R/R AML) and HR-MDS.

BH-30236 is being evaluated in a Phase 1/1b multicenter, open-label, first-in-human dose escalation and expansion trial in adults with R/R AML and HR-MDS. The U.S. Food and Drug Administration has granted orphan drug designation to BH-30236 for the treatment of AML.

(Press release, BlossomHill Therapeutics, MAY 12, 2026, View Source [SID1234665580])

On May 12, 2026 Tevogen ("Tevogen Bio Holdings Inc." or "Company") (Nasdaq: TVGN) reported that it has entered into a securities purchase agreement for a private investment in public equity (the "PIPE") financing with existing investor The Patel Family, LLP for gross proceeds of $3 million. The Company intends to use the proceeds from the PIPE financing to support ongoing operations, advance strategic growth initiatives, and for general corporate purposes.

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Pursuant to the terms of the securities purchase agreement, Tevogen will issue 375,000 prefunded warrants each exercisable for the purchase of one share of the Company’s common stock. The PIPE financing was priced at $8.00 per prefunded warrant, which represents a 14% premium to the closing price of the Company’s stock on May 11, 2026. The PIPE financing is expected to close on or about May 13, 2026.

"Having The Patel Family, LLP continue to support Tevogen reflects a shared belief in both our mission and our long-term vision for building a more accessible and sustainable healthcare model," said Tevogen Bio founding CEO Ryan Saadi, MD, MPH. "We believe this financing along with an existing ATM offering and loan agreement, provides the company with access to adequate capital to reach revenue milestones."

"Our continued investment emphasizes our conviction in Tevogen, its leadership and novel technology, and we look forward to being long-term holders," said investor Dr. Manmohan Patel, MD, on behalf of The Patel Family, LLP.

The securities issued in the PIPE financing have not been registered under the Securities Act of 1933, as amended, or applicable state securities laws. Accordingly, the securities may not be reoffered or resold in the United States except pursuant to an effective registration statement or an applicable exemption from the registration requirements of the Securities Act and such applicable state securities laws. In connection with the private placement, the Company has agreed to file a registration statement with the U.S. Securities and Exchange Commission covering the resale of the shares issuable upon exercise of the prefunded warrants.

This press release shall not constitute an offer to sell or the solicitation of an offer to buy any securities, nor shall there be any sale of these securities in any jurisdiction in which such offer, solicitation, or sale would be unlawful prior to the registration or qualification under the securities laws of any such jurisdiction.

(Press release, Tevogen Bio, MAY 12, 2026, View Source [SID1234665579])

On May 12, 2026 BridgeBio Oncology Therapeutics, Inc. ("BBOT") (Nasdaq: BBOT), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, reported financial results for the first quarter ended March 31, 2026, and provided a business update, including highlights of pipeline progress.

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BBOT’s portfolio of late-stage RAS-pathway inhibitors is designed to enable direct dual inhibition of KRAS in both its ON and OFF states, pan-KRAS coverage across major KRAS mutations, and disruption of RAS-driven PI3Kα activation. Together, these assets uniquely position BBOT to achieve safe, concurrent, high-level suppression of both the MAPK and PI3Kα pathways through a wholly owned internal combination strategy.

"In the first quarter, we reported meaningful progress across all three clinical programs, including encouraging preliminary antitumor activity and a potentially differentiated safety profile for BBO-8520 in lung cancer; anti-tumor activity and a partial response (PR) in pancreatic cancer with BBO-11818 as monotherapy; and confirmation of full target engagement without hyperglycemia for BBO-10203," said Pedro J. Beltran, PhD, Chief Executive Officer of BBOT. "In addition, we announced the publication of BBO-11818 in Cancer Discovery, highlighting its role as a potent and selective pan-KRAS inhibitor. These results and our cash runway into 2028 position us well as we continue advancing our differentiated pipeline to provide new treatment options for patients with limited choices."

Key Clinical Highlights & Upcoming Milestones

BBO-8520: An orally bioavailable small molecule direct inhibitor targeting both the ON and OFF states of KRAS.

On January 7, 2026, BBOT announced new clinical data from the ongoing Phase 1 ONKORAS-101 trial (NCT06343402).
As of November 15, 2025, BBO-8520 monotherapy in patients with KRASG12C non-small cell lung cancer (NSCLC) showed a 65% objective response rate (ORR) and a 68% 6-month progression-free survival (PFS), with 83% of patients eligible for 6-month follow-up remaining on treatment for ≥6 months, alongside a potentially differentiated safety profile.
BBO-8520 in combination with pembrolizumab demonstrated promising efficacy data and a distinct safety profile at active dose levels, including a potentially differentiated liver toxicity profile.
An internal combination study with BBO-10203 opened in April 2026.
Updated clinical data from the combination trial with pembrolizumab are expected in the second half of 2026.

BBO-11818: An orally bioavailable small molecule pan-KRAS inhibitor that targets mutant KRAS in both the ON and OFF states.

On January 7, 2026, BBOT announced preliminary clinical data from the ongoing Phase 1 KONQUER-101 trial (NCT06917079) for advanced solid tumors. BBO-11818 demonstrated encouraging early anti-tumor activity across dose levels and tumor types, including a PR in a patient with pancreatic ductal adenocarcinoma (PDAC) with a 56% tumor reduction. BBO-11818 monotherapy appeared generally tolerable with no dose-limiting toxicities (DLTs).
On March 6, 2026, BBOT announced the publication of preclinical data describing the discovery and characterization of BBO-11818 in Cancer Discovery, a peer-reviewed journal of the American Association for Cancer Research (AACR) (Free AACR Whitepaper). The paper, titled "Discovery of BBO-11818, a Potent and Selective Non-covalent Inhibitor of (ON) and (OFF) KRAS with Activity Against Multiple Oncogenic Mutants," details the foundational science underlying BBOT’s pan-KRAS inhibitor program.
Updated clinical data are expected in the second half of 2026. An internal combination study with BBO-10203 is anticipated to open later in 2026.

BBO-10203: An orally bioavailable small molecule with a novel mechanism of action designed to block the physical interaction between RAS and PI3Kα, inhibiting RAS-driven PI3Kα-AKT signaling in tumors.

On January 7, 2026, BBOT announced preliminary clinical data from the ongoing Phase 1 BREAKER-101 trial (NCT06625775).
BBO-10203 demonstrated a differentiated safety profile with no hyperglycemia in patients without restrictions on baseline HbA1c and glucose levels.
In addition, BBO-10203 achieved target systemic exposure and rapid full target engagement.
Clinical benefit was observed in patients with colorectal cancer (CRC) (>80% 3L+) and hormone receptor positive breast cancer (HR+ BC) who were previously heavily treated and tumor reductions were observed in some patients.
Updated clinical data are expected in the second half of 2026 and internal combination studies are anticipated to open in 2026.

Other Key Corporate Updates

In March 2026, Peter F. Lebowitz, MD, PhD, was appointed to BBOT’s Board of Directors. Dr. Lebowitz is Chief Executive Officer and Chief Medical Officer at Third Arc Bio. Previously, he served as Global Head of Oncology R&D at Johnson & Johnson (J&J), where he delivered 13 new drugs to market with over 60 approvals and 12 FDA Breakthrough Therapy Designations. Prior to J&J, he held senior oncology leadership roles at GlaxoSmithKline, where he filed 10 IND applications and advanced two medicines through global registration trials.
Subsequent to the end of the quarter, BBOT announced the appointment of Pedro J. Beltran, PhD, as Chief Executive Officer and Idan Elmelech as Chief Operating Officer, effective April 20, 2026. In addition, Neil Kumar, PhD, was appointed as the Executive Chairman of the Board of Directors and former CEO, Eli Wallace, PhD, will serve as a Senior Adviser to BBOT.

First Quarter 2026 Financial Results

Cash Position: As of March 31, 2026, BBOT had cash, cash equivalents and marketable securities totaling $388.9 million, which is expected to provide cash runway into 2028.
Research and development (R&D) expenses: R&D expenses were $39.8 million for the first quarter of 2026 compared to $20.6 million for the first quarter of 2025. The increase in expenses was primarily due to increases in clinical trial expenses and manufacturing expenses for BBO-8520, BBO-11818, and BBO-10203.
General and administrative (G&A) expenses: G&A expenses were $6.4 million for the first quarter of 2026 compared to $2.5 million for the first quarter of 2025. Changes in G&A expenses reflect the initiation of BBOT’s standalone operations and de-SPAC transaction.
Net Loss: Net loss was $42.1 million for the first quarter of 2026 compared to $22.1 million for the first quarter of 2025.

(Press release, BridgeBio Oncology Therapeutics, MAY 12, 2026, View Source [SID1234665578])