On April 22, 2026 BeyondSpring Inc. (NASDAQ: BYSI) reported new preclinical data at the 2026 Annual Meeting of the American Association for Cancer Research (AACR) (Free AACR Whitepaper) demonstrating that Plinabulin has the potential to enhance both the efficacy and tolerability of ADC therapy — potentially boosting anticancer responses while keeping patients on treatment long enough to benefit.

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Antibody-drug conjugates — a form of targeted chemotherapy that delivers cancer-killing agents directly to tumor cells, known as ADCs — have emerged as one of oncology’s most important new treatment classes. But two persistent clinical barriers limit their full potential: they do not always produce durable responses, and neutropenia (a dangerous drop in white blood cell counts) can force dose reductions or treatment delays that cut treatment short. New AACR (Free AACR Whitepaper) data show that Plinabulin directly and simultaneously addresses both.

Three Key Findings from AACR (Free AACR Whitepaper) 2026

The data show why the combination works. Plinabulin, when added to two leading approved ADCs — T-DXd (trastuzumab deruxtecan) and Dato-DXd (datopotamab deruxtecan) — produced three significant results that neither drug achieved alone:

Stronger anticancer activity: Complete tumor regressions were more frequent and animals survived significantly longer — in both two-drug (ADC+ Plinabulin) and three-drug (ADC+ Plinabulin + PD-1 inhibitor) combinations (PD-1 inhibitors are immunotherapies that activate the body’s own immune system to fight cancer).
Better tolerability to potentially keep patients on therapy: Plinabulin reduced animal death in both two-drug and three-drug combinations. In 6 prior clinical studies, Plinabulin measurably reduced chemotherapy-induced neutropenia, the white blood cell toxicity that commonly forces ADC dose reductions or treatment delays — potentially allowing patients to remain on treatment long enough to benefit from the drug’s anticancer activity.
Immune system activation: Analysis showed that Plinabulin enhanced the body’s own cancer-fighting T-cells, significantly increasing CD8+ T cell/Treg ratio — providing a biological explanation for why the combination outperforms either drug alone.

Plinabulin is Mechanistically Complementary, Not Merely Additive

Plinabulin activates a protein called GEF-H1 that simultaneously matures immune cells (dendritic cells) to attack tumors, signals the body to replenish cancer-fighting blood cells, and disrupts the blood supply feeding tumors. These are precisely the biological pathways that ADCs do not activate — which is why the two work better together than either does alone.

In BeyondSpring’s pivotal Phase 3 DUBLIN-3 study (The Lancet Respiratory Medicine, 2024), Plinabulin combined with docetaxel chemotherapy doubled two- and three-year survival rates in second- and third-line EGFR wild-type NSCLC patients — and simultaneously reduced docetaxel-limiting grade 4 neutropenia from 33% to 5%, keeping patients on therapy longer for the drug to work. The new AACR (Free AACR Whitepaper) data extend that same combination logic into the ADC setting, broadening Plinabulin’s reach across the treatment landscape.

BeyondSpring’s planned DUBLIN-4 program — a 442-patient FDA-aligned confirmatory Phase 3 trial building directly on the DUBLIN-3 results — is the defined next clinical step. Today’s AACR (Free AACR Whitepaper) data further strengthen the scientific rationale for Plinabulin’s combination potential and point toward future ADC combination studies beyond the confirmatory program.

Plinabulin as a Potential Backbone Drug Across Multiple ADC Combinations

ADCs are increasingly being tested in earlier lines of cancer treatment and in combination with immunotherapy. However, recent large Phase 3 studies — TROPION-Lung01 and EVOKE-01 — showed that leading ADCs failed to outperform older chemotherapy, such as docetaxel, in certain lung cancer settings, underscoring the need for an agent that can improve the efficacy and tolerability of ADC-based combinations.

Plinabulin’s ability to simultaneously boost efficacy and reduce toxicity positions it as a potential backbone agent across the ADC landscape — a role no other drug currently fills. Today’s AACR (Free AACR Whitepaper) data open the door to ADC combination studies as a natural next chapter in Plinabulin’s clinical development, alongside the ongoing DUBLIN-4 confirmatory program.

"Plinabulin has the potential to enable ADC therapy to deliver on its full promise — producing more complete responses, extending survival, and keeping patients on treatment. These AACR (Free AACR Whitepaper) data further strengthen our conviction in Plinabulin’s combination potential, as we advance the DUBLIN-4 confirmatory Phase 3 program in NSCLC post immune checkpoint inhibitors and explore the broader opportunity in ADC-based regimens."
— Dr. Lan Huang, Co-Founder, Chairman, and CEO, BeyondSpring Inc.

BeyondSpring’s China operations have been a strategic engine in building the ADC partnerships that support Plinabulin’s global development.

"China’s ADC research ecosystem is among the most active in the world, and BeyondSpring is well-positioned to leverage those capabilities. Our collaboration with Shanghai Chest Hospital demonstrated the value of strategic partnerships in advancing Plinabulin’s preclinical and clinical development in ADC combination, and we see continued opportunity to build on that model as the ADC combination landscape evolves."
— Min Qiu, Deputy General Manager, BeyondSpring China

BeyondSpring’s AACR (Free AACR Whitepaper) 2026 Presentation

Title: Plinabulin Boosts Antitumor Efficacy of Topoisomerase Inhibitor-Based Antibody-Drug Conjugates Without or With Immune Checkpoint Inhibitor

Presenters: Yingjuan June Lu, Xiaoyan He, Weiwei Cheng, Zhengyan Zhang, James Tonra, Lan Huang

Session: T Cell Engagers 2 / Antibody-Drug Conjugates 1 (Immunology Track)

Poster Number: 5597

About Plinabulin

Plinabulin is a late-stage Phase 3 anticancer agent and first-in-class GEF-H1 (guanine nucleotide exchange factor H1) agonist. Its multifunctional mechanism — encompassing dendritic cell maturation, tumor microenvironment modulation, anti-angiogenesis, and chemotherapy-induced neutropenia (CIN) mitigation — activates biological pathways that standard chemotherapy and ADCs do not. Over 700 cancer patients have been treated with good tolerability and durable anticancer benefit in rational combination settings. DUBLIN-3 Phase 3 results in NSCLC were published in The Lancet Respiratory Medicine in 2024.

About DUBLIN-3 and the Path to DUBLIN-4

In the DUBLIN-3 Phase 3 study of 2L/3L EGFR wild-type NSCLC (Lancet Respiratory Medicine, 2024), Plinabulin plus docetaxel significantly outperformed docetaxel monotherapy (n=559, 1:1 randomization), with improvements in OS, PFS, and ORR; doubling of 2- and 3-year survival rates; and reduction of docetaxel-induced grade 4 neutropenia from 33% to 5% (p<0.0001).

DUBLIN-4 is BeyondSpring’s planned FDA-aligned confirmatory Phase 3 program (n=442, 1:1 randomization), designed to validate the DUBLIN-3 results in a prospective confirmatory setting in a patient population selected based on Plinabulin’s mechanism of action: non-squamous NSCLC patients who have progressed on PD-1/L1 inhibitors. The ADC preclinical data presented at AACR (Free AACR Whitepaper) 2026 broaden the scientific case for Plinabulin’s combination potential.

(Press release, BeyondSpring Pharmaceuticals, APR 22, 2026, View Source [SID1234664715])

On April 22, 2026 The US Food and Drug Administration (FDA) reported that it has extended by up to three months the target action date for its review of the biologics license application for Sarclisa (isatuximab-irfc) subcutaneous (SC) in combination with approved standard-of-care regimens for the treatment of patients with multiple myeloma (MM) across all currently approved US indications of Sarclisa intravenous (IV) formulation. The revised target action date for the FDA decision is July 23, 2026.

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Sanofi is committed to working closely with the FDA to bring this new advancement to patients and providers as quickly as possible. If approved, Sarclisa would be the first anticancer treatment to be administered through an on-body injector (OBI).

On March 26, 2026, the European Medicine Agency Committee for Medicinal Products for Human Use (CHMP) adopted a positive opinion recommending the approval of Sarclisa SC administered via both an OBI and manual injection for the treatment of MM patients across all currently approved indications and combinations for Sarclisa IV formulation in the EU. A final decision is expected in the coming months.

About Sarclisa
Sarclisa (isatuximab-irfc) has been approved in almost 60 countries across four indications for certain patients with newly diagnosed MM and relapsed or refractory MM. Sarclisa-based regimens have been prescribed to treat more than 60,000 patients worldwide.

At Sanofi, we are building on a long-standing commitment to oncology as we continue to chase the miracles of science to improve the lives of those living with cancer. We are committed to transforming cancer care by developing innovative, first and best-in-class immunological and targeted therapies for rare and difficult-to-treat cancers with high unmet need.

For more information on Sarclisa clinical studies, please visit www.clinicaltrials.gov.

(Press release, Sanofi, APR 22, 2026, View Source [SID1234664714])

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])