CN-201

SAN DIEGO, April 20, 2026 /PRNewswire/ -- Abogen, a clinical-stage biotechnology company focused on RNA innovation, today announced preliminary clinical results from the first-in-human (FIH) study of ABO2203 in patients with relapsed/refractory B-cell non-Hodgkin lymphoma (R/R B-NHL). The data were presented in an oral session delivered at the AACR Annual Meeting 2026 in San Diego by Professor Li Wang of Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine. ABO2203 is a lipid nanoparticle (LNP)-formulated mRNA drug candidate encoding a CD3×CD19 bispecific T-cell engager (TCE). By enabling in vivo TCE expression via mRNA, ABO2203 is designed to mitigate cytokine release syndrome (CRS) while maintaining robust clinical efficacy. The Key to TCE Therapies: Overcoming CRS Toxicity Nearly all marketed protein-based TCEs carry black-box warnings for CRS, which remains a primary safety challenge in the development of such therapies. While step-up dosing strategies are commonly used to reduce CRS risk, their effectiveness remains limited: Grade 2 CRS still occurs on average in 13%-22% of patients, with some cases requiring hospitalization or even ICU admission. In addition, from the standpoint of drug development, 2-3 years are typically required for dose-finding to determine an appropriate step-up dosing regimen. These challenges are further amplified when extending TCE therapies beyond oncology into autoimmune diseases. Patients with autoimmune conditions often exhibit heightened immune responsiveness and lower tolerance for adverse events, further raising the safety threshold. Moreover, given the chronic and generally non-life-threatening nature of these diseases, CRS-related risks present significant clinical barriers, particularly in outpatient settings. In autoimmune diseases where long-term disease stability depends on treatment safety, a favorable safety profile may represent a more meaningful competitive advantage than efficacy alone. Initial Clinical Data: Proof of Concept Validated, with Unlimited Potential The first‑in‑human trial of ABO2203 in R/R B‑NHL is a dose‑escalation and expansion study. The presentation included data from nine patients in the dose- escalation stage. Patients had received a median of four prior lines of therapy, and all had failed prior CD20‑targeted therapy. ABO2203 was administered subcutaneously across dose levels ranging from 3 μg to 1,920 μg. The maximum tolerated dose (MTD) has not yet been reached. Exceptional Safety Profile: ABO2203 was well tolerated across all evaluated dose levels. No dose‑limiting toxicities (DLTs), CRS, or ICANS were observed. Elevations in liver enzyme elevations were limited to Grade 1 and occurred at low incidence. The most common adverse event was Grade 1–2 pyrexia, without clinically significant changes in oxygen saturation or blood pressure. Grade 3/4 events were infrequent and primarily hematologic, with no unexpected safety signals beyond those associated with the TCE class or NHL. Favorable Pharmacokinetics and Pharmacodynamics: TCE expression was detected across all three dose cohorts. The time to peak concentration was gradual after each administration (Tmax = 5.5 days), with a half‑life of 7.9 days. These findings support an initial once-weekly dosing regimen, with the potential to extend dosing intervals to every two weeks following response, and possibly every three to four weeks thereafter. In contrast to the "pulse‑like" pharmacokinetic profile of protein‑based TCEs, the mRNA‑expressed TCE demonstrated a flatter and more sustained exposure profile. Compared with a protein TCE of identical amino acid sequence (P4107), which reached peak levels and was eliminated rapidly, ABO2203 exhibited a delayed peak TCE concentration and prolonged half-life. The lower peak concentration (Cmax) may help mitigate cytokine release, while sustained mRNA expression may contribute to more durable anti-tumor efficacy than P4107. Encouraging Efficacy Signals: Based on Lugano 2014 criteria, objective response rates (ORR) were dose-dependent across cohorts, reaching 33%, 67%, and 100% in the low-, medium-, and high-dose groups, respectively. Complete metabolic responses (CMRs) were observed in both the medium- and high-dose cohorts, with a 100% complete response (CR) rate achieved in the high-dose cohort as updated by Professor Li Wang. Responses were seen across both aggressive (DLBCL) and indolent (FL, MCL, MZL) lymphomas, with a 100% ORR in follicular lymphoma. Compelling Clinical Significance and Commercial Potential These findings provide initial clinical proof of concept (PoC) for mRNA-encoded TCE therapeutics, demonstrating a superior safety profile, favorable pharmacodynamics, and encouraging efficacy in B-NHL. The data also suggest potential applications in autoimmune diseases. ABO2203's ability to effectively deplete B cells within lymph nodes may address a well-recognized limitation of conventional CD19/CD20 monoclonal antibodies and existing TCEs in these indications. The results come amid growing momentum in the TCE field. Since late 2024, the sector has seen increased deal activity, including Merck's USD 1.3 billion acquisition of CN201 (CD3/CD19) and GSK's USD 300 million upfront licensing of Chimagen's trispecific TCE. More recently, Gilead announced a USD 1.675 billion upfront acquisition of Ouro Medicines and its CD3/BCMA bispecific asset, CM336/OM336 this March. With the global TCE market projected to reach USD 121 billion by 2035 (Frost & Sullivan), ABO2203 represents a promising asset in this rapidly expanding category. About Abogen Abogen is a clinical-stage biotechnology company dedicated to developing novel medicines based on RNA technologies. Founded in 2019, the company has established integrated in-house capabilities spanning the full mRNA development lifecycle, including protein engineering, mRNA sequence design and synthesis, lipid nanoparticle (LNP) delivery, formulation, and large-scale manufacturing. SOURCE Abogen 21% more press release views with Request a Demo

Merck (NYSE: MRK) has entered into a definitive agreement to acquire Terns Pharmaceuticals (Nasdaq: TERN), a clinical-stage oncology company, for USD 53.00 per share in an all-cash transaction valued at approximately USD 6.7 billion. The Merck Terns Pharmaceuticals acquisition positions the pharma company to consolidate its presence in hematology through TERN-701, an oral allosteric BCR::ABL1 tyrosine kinase inhibitor currently in Phase I/II development for chronic myeloid leukemia. The transaction represents approximately USD 5.7 billion net of acquired cash and carries a premium of 31% to the 60-day and 42% to the 90-day volume-weighted average stock price as of March 24, 2026. The deal contains no disclosed milestone payments, contingent value rights, or earn-out provisions. Merck will execute the acquisition through a tender offer requiring a majority of Terns stockholders to tender their shares, with closing expected in Q2 2026 following expiration of the Hart-Scott-Rodino waiting period. The transaction will be accounted for as an asset acquisition, resulting in an approximately USD 5.8 billion charge (approximately USD 2.35 per share) recognized in both Q2 and full-year 2026 GAAP and non-GAAP results. The asset acquisition classification means the acquired in-process R&D will be expensed immediately rather than capitalized. TERN-701: Mechanism and clinical status TERN-701 is a BCR-ABL1 tyrosine kinase inhibitor designed to bind to the ABL myristoyl pocket, an allosteric site distinct from the ATP-binding domain targeted by earlier-generation TKIs. CML is driven by the Philadelphia chromosome, a translocation between chromosomes 9 and 22 that produces constitutive activation of the BCR::ABL1 fusion protein, which fuels malignant white blood cell proliferation. The compound is being evaluated in the CARDINAL trial (NCT06163430), a global multi-center dose escalation and expansion study enrolling patients with Ph+ chronic phase CML who experienced treatment failure, suboptimal response, or intolerance to at least one prior TKI. The dose escalation portion completed in January 2025 with no dose-limiting toxicities observed up to 500 mg QD. Dose expansion initiated in April 2025 across two cohorts (320 mg and 500 mg QD), and in January 2026 an additional cohort was added to evaluate activity against BCR::ABL1 resistance mutations including T315I, M244V, and F359I/C/V. The FDA granted Orphan Drug Designation for TERN-701 in CML in March 2024. Clinical data reported to date indicate rates of major molecular response and deep molecular response by week 24, including in patients with high disease burden who had received multiple prior therapy lines, with low rates of severe adverse events and discontinuations. Specifically, Terns reported a 75% cumulative MMR rate by 24 weeks in 32 efficacy-evaluable patients. The strategic context The TERN-701 CML program joins a Merck hematology pipeline that already includes three Phase III candidates: bomedemstat (LSD1 inhibitor), nemtabrutinib (non-covalent BTK inhibitor), and zilovertamab vedotin (ROR1-targeting ADC), along with MK-1045 (CD19×CD3 T-cell engager) in Phase Ib/II. The Terns buyout extends a pattern of aggressive deal-making driven by the approaching Keytruda patent cliff (~2028). Merck’s recent transactions include the USD 9 billion purchase of influenza-focused Cidara Therapeutics, Inc. (Nasdaq: CDTX), the USD 10 billion purchase of Verona Pharma for a COPD therapy, and the USD 10.8 billion acquisition of immunology-focused Prometheus Biosciences. In the chronic myeloid leukemia treatment landscape, TERN-701 enters a competitive field. Novartis markets asciminib (Scemblix), the first approved allosteric BCR::ABL1 inhibitor, which received FDA approval in 2022 for Ph+ CML after two or more prior TKIs and gained a first-line CML indication based on the ASC4FIRST trial. Sun Pharma Advanced Research is developing denimsertib, another allosteric BCR::ABL1 inhibitor in clinical development. Earlier-generation ATP-competitive TKIs from Novartis (imatinib, nilotinib), Bristol Myers Squibb (dasatinib), and Pfizer (bosutinib) remain standards of care, though resistance mutations and tolerability limitations persist across these agents. Your email address will not be published. Required fields are marked * Comment * Name * Email * Website