On April 22, 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 new preclinical data presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, highlighting the discovery and characterization of its lead pan-KRAS inhibitor, BH-501284, along with additional updates across its pipeline.

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"Despite recent advances, patients with KRAS-driven tumors continue to face limited and often short-lived treatment options. Our mini-symposium presentation at AACR (Free AACR Whitepaper) introduces our differentiated pan-KRAS inhibitor, BH-501284, with pre-clinical data demonstrating the potential for this molecule to deliver broad and durable pathway inhibition across multiple KRAS-driven tumors," said Jean Cui, Ph.D., Founder and Chief Executive Officer of BlossomHill Therapeutics. "We are particularly encouraged by the depth and consistency of activity observed across models, including sustained target engagement and tumor regression at low dose levels. Based on these results, we are advancing IND-enabling studies for BH-501284 and preparing for clinical development."

Data presented in the AACR (Free AACR Whitepaper) Mini Symposium provides pre-clinical data supporting BH-501284 as a novel, orally available, non-covalent, pseudo-irreversible pan-KRAS inhibitor designed to overcome limitations of current KRAS-targeted therapies.

Key findings from the mini symposium titled "Discovery and characterization of BH-501284: A non-covalent, pan-KRAS inhibitor for treatment of diverse KRAS-mutant tumors" include:

Median IC50 of 0.83 nM across 41 different G12/G13 KRAS mutant cell lines (excluding G12R), but sparing HRAS and NRAS (>650 nM) to avoid the toxicity of pan-RAS inhibitors
Picomolar binding affinity and prolonged residence time (>54 hours) mirroring the binding of covalent inhibitors but with a non-covalent, pseudo-irreversible chemistry leading to prolonged inhibition of KRAS signaling
Deep tumor regression in multiple KRAS-mutant xenograft models achieved at lower doses (5-15 mg/kg BID) compared to what has been reported with other contemporary Switch-II pocket inhibitors
The company also presented a poster describing the preclinical characterization of additional molecules within the pan-KRAS program (BH-501242, BH-501352), in which BH-501242 demonstrated cellular potency exceeding that of comparator molecules, and both molecules demonstrated prolonged non-covalent binding, and favorable absorption, distribution, metabolism and excretion (ADME) properties.

Additional AACR (Free AACR Whitepaper) Posters from the BlossomHill Therapeutics Pipeline

BH-30643 (Mutant-selective EGFR inhibitor)
Poster: "BH-30643, a novel macrocyclic non-covalent, mutant-selective EGFR inhibitor, addresses the resistance and potency limitations of contemporary EGFR TKIs"

Potent and durable inhibition across diverse EGFR-mutant models, including C797S and T790M
Maintained low nanomolar potency in presence of EGFR ligands
Showed prolonged suppression of tumor cell growth compared to approved EGFR TKIs
Induced deep tumor regression across multiple in vivo models, including intracranial models
Sustained suppression of EGFR signaling in dose- and time-dependent manner
Findings support potential of BH-30643 to overcome key limitations of current therapies
BH-30236 (CLK inhibitor for hematologic malignancies)
Poster: "CLK inhibitor BH-30236 synergizes with venetoclax in anti-leukemia activity via splicing modulation in preclinical AML and CLL models"

Broad anti-proliferative activity through modulated mRNA splicing
Reduced expression of pro-survival factors, leading to activation of apoptosis and DNA damage response pathways
Consistent synergy with venetoclax across multiple blood cancer models
Induced tumor regression in resistant acute myeloid leukemia (AML) xenografts, including complete responses
Sustained tumor-free survival following treatment discontinuation, consistent with effects on leukemia stem cell populations
Findings support continued clinical development of BH-30236 as both a monotherapy and in combination regimens

(Press release, BlossomHill Therapeutics, APR 22, 2026, View Source [SID1234664713])

On April 22, 2026 EvolveImmune Therapeutics, a clinical-stage immuno-oncology company developing a new class of multi-specific T cell engagers with integrated CD2 costimulation, reported the presentation of new data highlighting its novel EVOLVE T cell engager platform and an update on its lead asset, EVOLVE104, at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting. The results presented included findings from collaborative research conducted in partnership with Michael L. Dustin, Ph.D., Kennedy Trust Professor of Molecular Immunology at the University of Oxford, UK. The AACR (Free AACR Whitepaper) conference is being held April 17-22, 2026, in San Diego, California.

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The EVOLVE platform is designed to therapeutically co-opt key mechanisms central to efficient immune synapse formation and T cell effector function. This approach aims to bypass low tumor immunogenicity, conditionally activate adaptive immunity and reduce T cell dysfunction, allowing for amplified and sustained T cell tumor killing capacity, to address unmet medical needs in solid tumors and hematologic malignancies.

"Our presentations at AACR (Free AACR Whitepaper) share an impressive collection of first-in-class scientific findings for the EVOLVE platform and the continued clinical progress of our EVOLVE104 program. We are unlocking new insights into the mode of action of our EVOLVE platform which are catalyzing new and impactful prospects for our pipeline growth," said Stephen Bloch, M.D., Chief Executive Officer of EvolveImmune. "Our focus remains on efficiently executing our ongoing clinical study for EVOLVE104, while advancing further differentiated innovation opportunities for our EVOLVE technology."

Highlights from the company’s presentations at the AACR (Free AACR Whitepaper) conference are as follows:

EVOLVE104:

EvolveImmune spotlighted its ongoing phase 1 clinical trial of EVOLVE104, the first molecule from the company’s EVOLVE platform to enter clinical development (presentation #CT079). The compound targets a novel set of tumor-associated antigens, ULBP2/5/6, which are expressed on bladder cancers and squamous cell carcinomas. Notably, EVOLVE104 is the first T cell-redirecting therapeutic candidate targeting ULBP2/5/6 to enter clinical development.

The phase 1a/1b study, EIU-104101 (NCT07217171), is evaluating the safety, efficacy, pharmacokinetics and pharmacodynamics of EVOLVE104. The trial, began enrolling in December 2025, is designed with an initial phase 1a dose escalation portion, to be followed by phase 1b dose expansion, enrolling up to 160 subjects with locally advanced or metastatic bladder cancer and squamous cell carcinomas of the lung, esophagus, skin, tongue, and anogenital region who have relapsed from or are refractory to standard of care therapies. The study is currently open at nine US sites, with additional sites expected to open during the remainder of 2026.

EVOLVE T Cell Engager Platform:

In an oral minisymposium presentation (presentation #4055), EvolveImmune shared updated results from preclinical studies demonstrating that EVOLVE’s integrated CD2 co-stimulation approach shows superiority to conventional CD3-bispecific T cell engagers. Chronic in vitro human T cell stimulation with EVOLVE demonstrated sustained activation and proliferation, as well as enhanced differentiation into more effective effector-memory T cells. This activity correlated with improved tumor-dependent cytotoxicity compared to conventional CD3-bispecific T cell engagers. Notably, this superior profile for EVOLVE was observed with primary human tumor-infiltrating lymphocytes as well.

The enhanced T cell activity driven by EVOLVE led to greater tumor growth inhibition in an in vivo lung tumor xenograft model, when compared to bispecific T cell engagers. These findings add to the growing collection of evidence demonstrating that integrated T cell CD2 costimulation mediated by EVOLVE molecules results in superior human T cell performance compared to conventional CD3-bispecific T cell engagers.

A second poster presentation (presentation #5594) described experimental results conducted in collaboration with the laboratory of Professor Dustin. These findings showed that the EVOLVE platform functionally mimics the naturally occurring processes involved in human T cell recognition of target cells for their activation. This includes the active generation of an immune interface, or immune synapse, between T cells and target cells, which includes the positioning of CD2 to the corolla of the synapse, a hallmark feature of this interface. This activity correlated with increased T cell receptor signaling, improved T cell fitness and greater tumor killing. These findings provide further insight into the fundamental mechanistic activity that mediates the ability of EVOLVE to enhance T cell-mediated anti-tumor activity.

"It is remarkable how well EVOLVE mimics synaptic patterns generated by natural CD58 in a target membrane," said Professor Dustin.

About EVOLVE104
EVOLVE104 is a next-generation trispecific T cell engager that binds CD3 and CD2 on T cells and the tumor-associated antigens ULBP2/5/6, which have limited expression in normal human tissues and are found on a number of epithelial-derived malignancies, including urothelial carcinoma and a broad array of squamous cell carcinomas. In preclinical studies, EVOLVE104 has demonstrated compelling single-agent activity and combination activity with anti-PD-1 therapy, the ability to reinvigorate dysfunctional T cells, and a promising safety profile. EVOLVE104 is currently being studied in a first-in-human phase 1 clinical trial in subjects with advanced, relapsed or refractory solid tumors (NCT07217171).

(Press release, EvolveImmune Therapeutics, APR 22, 2026, View Source [SID1234664712])

On April 22, 2026 Sironax, a global clinical-stage biotechnology company developing transformative therapies for neurodegenerative, inflammatory and immunological, metabolic, and rare diseases, reported the selection of an abstract for presentation in a poster session at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) annual meeting. The meeting will take place from May 29 to June 2 in Chicago, IL.

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Presentation details are below:

Poster Title: SARM1 Inhibition to Prevent Chemotherapy-Induced Peripheral Neuropathy: Translational and Early Clinical Evaluation of SIR2501
Poster Board: 131
Abstract #: 12148
Date/Time: May 30, 2026, 1:30-4:30 PM CDT

(Press release, Sironax, APR 22, 2026, View Source [SID1234664711])

On April 22, 2026 SEED Therapeutics, Inc. ("SEED"), a clinical-stage biotechnology company pioneering rationally designed molecular glue degraders, reported new data demonstrating potent anticancer activity of its RBM39 degrader program in neuroblastoma, a pediatric cancer with high unmet medical need. SEED’s scientific work also identified potential biomarkers predictive of anticancer response that will be further examined in the clinic, with Phase 1 dose escalation projected to be completed by Q1 2027. The findings are being presented at the 2026 Annual Meeting of the American Association for Cancer Research (AACR) (Free AACR Whitepaper), which convenes more than 22,000 scientists, clinicians, and investors this week in San Diego.

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ST-01156, SEED’s clinical-stage RBM39 molecular glue degrader, is currently being evaluated in a Phase 1 dose escalation study (NCT07197554) at six leading U.S. oncology centers.

Highlights At A Glance

Tumor eradication in a rigorous in vivo model: ST-01156 achieved complete tumor regression in neuroblastoma model using a differentiated dosing regimen — a demanding efficacy benchmark in solid tumor oncology.
Active Phase 1 clinical trial: Dose escalation is underway (NCT07197554) at six leading U.S. oncology centers, with clinical sites in additional geographies in preparation.
Biomarker strategy: MYC overexpression (sensitivity) and CDKN2A/B deletion (resistance) were identified as part of SEED’s biomarker program, potentially enabling precision patient enrollment as the trial advances.
Rare Pediatric and Orphan disease opportunity: Neuroblastoma is a high-unmet-need rare pediatric cancer representing a Rare Pediatric Disease and Orphan Disease designation-eligible indication, with potential for expedited regulatory pathways including Priority Review Voucher eligibility.

Scientific Rationale: Why RBM39 Matters

RBM39 is an RNA-binding protein that governs pre-mRNA splicing — a process cancer cells exploit to fuel uncontrolled growth, evade cell death, and repair DNA damage. By degrading RBM39 entirely, rather than merely inhibiting it, SEED’s approach disrupts multiple oncogenic pathways simultaneously: cell cycle progression, metabolic reprogramming, DNA damage response, and programmed cell death (apoptosis — the process by which damaged or cancerous cells are eliminated by the body). This breadth of effect is a key differentiator from conventional targeted therapies.

Molecular glue degraders achieve this by redirecting the cell’s own quality-control machinery — the ubiquitin-proteasome system — to tag and destroy the target protein. SEED’s proprietary RITE3 platform was designed from inception to identify, validate, and optimize molecular glues with a defined therapeutic window, bringing rational drug design to protein targets previously considered undruggable.

Key Data Highlights — AACR (Free AACR Whitepaper) 2026 Poster #5785

Tumor eradication in an in vivo model: ST-01156 achieved complete tumor regression in a neuroblastoma xenograft model — meaning tumors disappeared entirely — using the same dosing schedule now deployed in the Phase 1 trial. This direct correspondence between preclinical and clinical dosing strengthens confidence in the translational path forward.
Consistent potency across a biologically diverse disease: ST-01156 demonstrated potent anticancer activity across ten neuroblastoma models — six established cell lines and four patient-derived models — with IC50 values (the concentration required to kill half of cancer cells) in the low-to-sub-micromolar range. Neuroblastoma is genetically heterogeneous; this breadth of coverage matters.
A clear mechanism of action: Treatment with ST-01156 induced DNA damage, switched on the tumor-suppressing p53/p21 pathway, and reduced the levels of known cancer-driving proteins cMYC and EZH2 — confirming a coherent, multi-pronged path to programmed cancer cell death (apoptosis).
Biomarker roadmap for precision enrollment: SEED’s translational research identified MYC overexpression as a marker of sensitivity to ST-01156, and CDKN2A/B deletion as a marker of resistance. These biomarkers — identifiable through standard tumor profiling — may provide a practical framework for selecting patients most likely to benefit as the Phase 1 trial progresses toward expansion cohorts.

"ST-01156’s advancement into clinical testing in 2026 marks a pivotal milestone for SEED and for patients with RBM39 dependent cancers, including neuroblastoma — a pediatric cancer with very limited effective treatment options. The identification of MYC and CDKN2A/B status as potential biomarkers is the product of SEED’s focus on identifying the patients who will significantly benefit from ST-01156."

— James Tonra, PhD, President & Chief Scientific Officer, SEED Therapeutics

"The RBM39 data we are presenting at AACR (Free AACR Whitepaper) 2026 reflect what SEED’s RITE3 platform was designed to do — not just degrade a difficult target, but understand which patients are most likely to benefit. Seeing ST-01156 achieve complete tumor regression in a neuroblastoma model, at the same dosing schedule now in the clinic, is deeply gratifying and scientifically meaningful. Our focus at SEED is on ensuring that the molecular insight behind this program translates into real outcomes for patients with very few options."

— Lan Huang, PhD, Co-Founder, SEED Therapeutics

Clinical Development Status

ST-01156 is being evaluated in an ongoing Phase 1 dose escalation study (NCT07197554) designed to establish safety, pharmacokinetics, and target engagement. The study enrolls patients enriched for cancer types with demonstrated RBM39 dependency in preclinical research. The trial is currently active at six leading U.S. oncology centers, with additional clinical sites in preparation. Phase 1 dose escalation is projected to be completed by Q1 2027. The dosing schedule employed is consistent with that used in IND-enabling studies and in the in vivo efficacy program reported at AACR (Free AACR Whitepaper) 2026 — providing a robust translational foundation.

AACR 2026 Poster Presentation Details

Title: RBM39 Degrader Anticancer Activity Against Neuroblastoma; MYC and CDKN2A/B as Potential Response Biomarkers
Poster Number: 5785
Session: Proximity-Induced Drug Discovery 2 (Experimental and Molecular Therapeutics)
Authors: James Finn, Imad Salhab, Haihong Jin, Fei Liu, Dong Liu, Yunkai Zhang, Xing Liu, James Tonra, Lan Huang, Dan Lu

(Press release, Seed Therapeutics, APR 22, 2026, View Source [SID1234664710])

On April 22, 2026 CytoDyn Inc. (OTCQB: CYDY) ("CytoDyn" or the "Company"), a clinical-stage oncology company advancing leronlimab, a first-in-class humanized monoclonal antibody targeting the CCR5 receptor with therapeutic potential across multiple indications, including metastatic triple-negative breast cancer ("mTNBC") and colorectal cancer ("mCRC"), reported that new clinical data from its ongoing Phase 2 study in metastatic colorectal cancer (mCRC) were presented at the AACR (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22, 2026, at the San Diego Convention Center.

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The presentation highlighted findings supporting CCR5 inhibition with leronlimab as a strategy to modulate the tumor microenvironment, enhance immune engagement, and improve outcomes in metastatic colorectal cancer (mCRC), particularly in combination with standard-of-care therapies.

Metastatic colorectal cancer remains a significant clinical challenge, particularly in patients with refractory disease who have progressed on multiple prior lines of therapy. While standard regimens such as TAS-102 in combination with bevacizumab provide modest benefit, treatment resistance and immune evasion continue to limit durable responses. Results presented at AACR (Free AACR Whitepaper) demonstrate that CCR5 inhibition with leronlimab may enhance anti-tumor activity by modulating the tumor microenvironment and improving immune engagement.

"Preliminary results from our ongoing Phase 2 study suggest that CCR5 inhibition with leronlimab may enhance both biomarker and clinical responses in heavily pretreated mCRC patients," said Pashtoon M. Kasi, M.D., M.S., Medical Director of GI Oncology, City of Hope Orange County, Irvine, California. "Real-time assessment of novel liquid biopsy biomarkers, including circulating tumor cells, circulating tumor DNA, and cancer-associated macrophage-like cells in blood, along with integrated evaluation of tumor tissue and the tumor microenvironment, is providing insights that conventional imaging and traditional assessment methods cannot capture."

Key findings from the ongoing Phase 2 mCRC study include:

Among pre-screened patients with evaluable samples (N=33), CCR5 expression was detected in 100% of cases, supporting its potential as a therapeutic target in mCRC.
Early clinical and biomarker responses were observed, including rapid and substantial reductions in circulating tumor DNA (ctDNA), with median declines of approximately 70% by week 2 across evaluable patients (N=19).
The combination regimen has been well tolerated, with no leronlimab-related dose-limiting toxicities (DLTs) observed, and escalation to 700 mg dosing underway.
The study continues to enroll toward full enrollment, reflecting significant unmet need in previously treated mCRC.
"Building on the translational and clinical data presented earlier in the week in mTNBC, these findings further support CCR5 as a key regulator of the tumor microenvironment across solid tumors," said Jacob P. Lalezari, M.D., Chief Executive Officer of CytoDyn. "The early biomarker and clinical signals observed in our ongoing Phase 2 mCRC study reinforce the potential of leronlimab-based combination approaches to enhance immune engagement and address resistance in heavily pretreated patients."

The poster presentation titled "Preliminary results of a phase 2 study of leronlimab in combination with TAS-102 and bevacizumab in previously treated metastatic colorectal cancer" was presented by Dr. Kasi on April 21, 2026, from 2:00 p.m. – 5:00 p.m. PT (Poster #6466). A copy of the poster will be made available on CytoDyn’s website under the Publications & Posters section.

(Press release, CytoDyn, APR 22, 2026, View Source [SID1234664709])