On April 15, 2026 TRIANA Biomedicines, Inc. (TRIANA), a leading biopharmaceutical company focused on advancing a target-first and proximity-first molecular glue discovery platform to address difficult to drug disease targets, reported one oral and three poster presentations regarding the Company’s clinical asset, TRI-611, as well as its preclinical asset Cyclin E1 (CCNE1) will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17-22, 2026 in San Diego, California.

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TRIANA will present data highlighting the first-in-class clinical stage compound TRI-611 as a selective, brain-penetrant molecular glue degrader for the treatment of anaplastic lymphoma kinase–positive (ALK+) non-small cell lung cancer (NSCLC). In pre-clinical ALK+ NSCLC tumor models, TRI-611 promotes the degradation of tyrosine kinase inhibitor (TKI)-sensitive and -resistant ALK fusion proteins and leads to regression of both ALK TKI-refractory subcutaneous and intracranial tumors. TRI-611 demonstrates combinability with ALK TKIs in pre-clinical tumor models, potentially opening additional therapeutic avenues for patients with ALK+ NSCLC.

"We are pleased to provide further preclinical data highlighting the breadth of our molecular glue degrader therapeutics portfolio," said Dr. Patrick Trojer, President and CEO of TRIANA. "By binding at a site distal to the TKI domain binding site, TRI-611 tethers the E3 ligase complex cereblon to ALK fusion proteins, promoting their destruction by engaging the cell’s own degradation machinery. This mechanism renders potent tumor regression activity, irrespective of mutations in the TKI binding domain."

Oral Presentation Details:

Title:

TRI-611, a potent, selective, CNS-penetrant ALK molecular glue degrader for the treatment of ALK-fusion protein positive non-small cell lung cancer

Abstract Number:

ND07

Date and Time:

Sunday, April 19, 2026, 3:45 p.m. – 4:00 p.m. PT

Session Category:

New Drugs on the Horizon: Part 2

Session:

DDT02

Location:

Ballroom 20 CD – Upper Level – Convention Center

Poster Presentation Details:

Title:

TRI-611, a development stage molecular glue degrader of ALK, promotes the degradation of TKI-resistant ALK fusion proteins and leads to regression of ALK TKI-refractory tumors

Abstract Number:

5787 / 14

Date and Time:

Tuesday, April 21, 2026, 2:00 p.m. – 5:00 p.m. PT

Session Category:

Proximity-Induced Drug Discovery 2

Session:

T09.04

Location:

Poster Section 15

Title:

TRI-611, a development stage molecular glue degrader of ALK for the treatment of ALK-positive NSCLC including central nervous system metastases​

Abstract Number:

4618 / 28

Date and Time:

Tuesday, April 21, 2026, 9:00 a.m. – 12:00 p.m. PT

Session Category:

Proximity-Induced Drug Discovery 1

Session:

ET09.03

Location:

Poster Section 18

Title:

Discovery of a selective molecular glue degrader of CCNE1 for the treatment of CCNE1-amplified solid tumors and CDK4/6i-resistant HR+/HER2- breast cancers

Abstract Number:

5789 / 16

Date and Time:

Tuesday, April 21, 2026, 2:00 p.m. – 5:00 p.m. PT

Session Category:

Proximity-Induced Drug Discovery 2

Session:

ET09.04

Location:

Poster Section 15

About TRI-611

TRI-611 is a novel oral, small-molecule, investigational therapy designed to target and degrade ALK fusion proteins in patients with ALK+ NSCLC. TRI-611 is a potent, brain-penetrant molecular glue degrader that brings ALK fusion proteins and the E3 ligase enzyme cereblon together through a unique binding mechanism that works independently of the ALK kinase active site and harnesses the body’s innate protein-degradation machinery to selectively eliminate the ALK fusion protein. TRI-611 is designed to overcome the limitations observed with currently available ALK inhibitors.

About CCNE1

CCNE1 (cyclin E1) is a key disease driver in CCNE1-amplified tumors and in a subset of HR+/HER2- breast cancers. As a critical regulator of the cell cycle, CCNE1 protein levels are tightly regulated to maintain control of cell growth in normal cells, while elevation of CCNE1 protein levels can lead to aberrant cell growth in cancer. CCNE1 has been difficult to drug with traditional approaches. Our novel oral, small-molecule molecular glue degraders of CCNE1 offer a unique approach to targeting this key cancer driver by harnessing the cell’s protein degradation machinery to substantially decrease excess CCNE1 and halt growth of CCNE1-dependent tumor cells.

(Press release, Triana Biomedicines, APR 15, 2026, View Source [SID1234664421])

On April 15, 2026 Mabwell (688062.SH), an innovation-driven biopharmaceutical company with a fully integrated industry chain, reported that the National Medical Products Administration (NMPA) has accepted the Investigational New Drug (IND) application for its innovative LILRB4/CD3 TCE bispecific antibody (R&D code: 6MW5311). The drug candidate is being developed for hematologic malignancies, specifically Acute Myeloid Leukemia (AML), Chronic Myelomonocytic Leukemia (CMML), and Multiple Myeloma (MM).

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6MW5311 is the world’s first innovative LILRB4/CD3 TCE bispecific antibody for which a clinical trial application has been submitted. It possesses broad prospects for clinical development and significant market potential. The U.S. IND application is currently in the pre-IND phase, with plans to formally submit it to the FDA in the second quarter of 2026.

6MW5311 is developed based on the T Cell Engager (TCE) technology platform and features a "2+1" asymmetric molecular structure. It simultaneously targets LILRB4 and CD3, forming an immunological synapse by bridging tumor cells and T cells, thereby activating T cells to efficiently kill tumors.

The molecule incorporates a unique steric hindrance design. This structure significantly reduces the binding activity of the CD3 antibody to T cells in the absence of tumor cells. T cells are specifically activated only when tumor cells are present, which substantially enhances safety while improving anti-tumor efficacy.

In vitro studies have demonstrated that 6MW5311 exhibits potent cytotoxic activity across multiple tumor cell lines and patient-derived samples. In vivo pharmacodynamic studies have shown that 6MW5311 achieves significant tumor inhibition in both LILRB4-high and LILRB4-low expressing AML tumor models. Notably, it achieved complete tumor clearance in high-expression models. Furthermore, 6MW5311 demonstrated a favorable safety profile in cynomolgus monkey safety evaluation models.

As a key technological approach for directly mobilizing T cells to kill tumors, TCE has shown significant clinical value in various lymphoma indications, with multiple products successfully launched. However, current treatments for AML and CMML primarily remain primarily limited to chemotherapy, hematopoietic stem cell transplantation, and targeted therapies for specific mutations; no TCE products have been approved for these indications to date.

About Acute Myeloid Leukemia (AML)
AML is a group of clonal malignant disorders originating from myeloid stem cells, characterized by high heterogeneity and mortality. Globally, approximately 172.4 thousand new cases of AML were diagnosed in 2022, with the number projected to reach 221.4 thousand by 2035, representing a compound annual growth rate (CAGR) of 1.94%. In China, approximately 30.8 thousand new AML cases were diagnosed in 2022, accounting for approximately 17.9% of the global total. The number is expected to reach 36.7 thousand by 2035, representing approximately 16.6% of the global total, with a CAGR of 1.36%.

About Chronic Myelomonocytic Leukemia (CMML)
CMML is a clonal hematopoietic stem cell disorder that shares overlapping features with both myelodysplastic syndrome (MDS) and Myeloproliferative Neoplasm (MPN). It is characterized by significant monocytosis in peripheral blood and carries an inherent risk of transformation to AML (approximately 15-20% within 3-5 years). CMML is a rare disease with an annual incidence of approximately 3-4 per 100,000, and currently lacks effective treatment options.

About Multiple Myeloma (MM)
MM is a clonal plasma cell malignancy characterized by the uncontrolled proliferation of monoclonal plasma cells in the bone marrow. This leads to the overproduction of abnormal immunoglobulins and subsequent end-organ damage, manifested as hypercalcemia, renal impairment, anemia, and bone lesions (collectively known as CRAB features). Globally, MM accounts for approximately 1%-2% of all cancers and about 10% of hematologic malignancies. The median age at diagnosis is approximately 69 years, with higher incidence rates observed in males and individuals of African descent. Over the past two decades, patient survival rates have significantly improved thanks to the application of proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies. However, MM remains largely incurable, and most patients experience multiple relapses during the course of the disease.

(Press release, Mabwell Biotech, APR 15, 2026, View Source;nmpa-accepts-ind-application-for-mabwells-innovative-lilrb4cd3-tce-bispecific-antibody-6mw5311-302744036.html [SID1234664406])

On April 15, 2026 Forlong Biotechnology, a clinical-stage biotech company focusing on developing transformative cytokine therapies for patients with severe unmet needs, reported that its FL115 Program has successfully completed technical transfer of manufacturing process and analytical methods by its manufacturing partner JOINN Biologics INC, and will soon initiate production of GMP batches to support upcoming pivotal clinical trial in nonmuscle invasive bladder cancer (NMIBC).

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FL115 is an engineered IL-15/IL15Rα-Fbody fusion protein, of which Fbody is a single-chain Fc engineered to maintain FcRn affinity while eliminating binding of FcγRs and complement systems, aiming to optimize protein half-life and biodistribution. FL115 drug substance and drug products have demonstrated superb stability and solubility at 20 mg/ml, as well as robust GMP manufacturing process with low cost.

A clinical study of FL115 (NCT07122414) in Bacillus Calmette-Guérin (BCG) unresponsive NMIBC has been ongoing. After 1st patient dosing in August 2024, 10 patients have been dosed with FL115 alone and 42 patients have been dosed with FL115 in combination with BCG so far, all through intravesical delivery.

"We are excited about the potential best-in-class profile of FL115 in BCG unresponsive NMIBC, supported by preliminary safety and efficacy data across multiple dose-levels," said Dong Wei, Ph.D., Chief Executive Officer of Forlong Biotechnology, "we are on track to have a robust clinical data set to discuss with regulatory authorities on our pivotal clinical trial design and registration plan by end of 2026. CMC readiness is an important pillar of the FL115 program and we greatly appreciate the expertise and effort of JOINN Biologics as our manufacturing partner. Together we will advance FL115 into the pivotal clinical stage for NMIBC in 2027."

About FL115

FL115 is an engineered IL-15/IL15Rα-Fbody fusion protein, aiming to enhance anti-tumor immunity via IL-15-mediated signaling on NK and CD8+ T cells while minimizing complexity from Fc. FL115 has demonstrated significant anti-tumor activities as a monotherapy or as part of combination therapy in vivo, and can be manufactured by a robust and efficient process with excellent product stability. Clinically, FL115 has demonstrated favorable safety profile and preliminary clinical responses as a monotherapy, and has the best-in-class potential to synergize with current and emerging T cell-targeting immunotherapies through combination therapy to significantly improve the treatment outcome for patients. It is currently being investigated in combination with Bacillus Calmette-Guérin (BCG) in a Phase 2 clinical trial to evaluate safety and preliminary efficacy in patients with nonmuscle invasive bladder cancer (NMIBC) and in combination with an anti-PD1 monoclonal antibody in a Phase 1b/2 clinical trial to evaluate safety and preliminary efficacy in patients with advanced solid tumors.

(Press release, Forlong Biotechnology, APR 15, 2026, View Source [SID1234664422])

On April 15, 2026 Mabwell (688062.SH), an innovative biopharmaceutical company with a full industry chain, reported that the National Medical Products Administration (NMPA) has accepted supplemental Biologics License Application for MAIWEIJIAN (denosumab injection, R&D code: 9MW0321), a product developed by its wholly-owned subsidiary T-mab, for the prevention of skeletal-related events in patients with multiple myeloma and in patients with bone metastases from solid tumors.

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MAIWEIJIAN is the first denosumab biosimilar (120mg) approved to market in China. It was initially approved in March 2024 for the treatment of adults and skeletally mature adolescents (defined as at least 1 mature long bone and weighing ≥ 45 kg) with giant cell tumor of bone that is unresectable or where surgical resection is likely to result in severe morbidity. In August 2025, the product received approval from the Drug Regulatory Authority of Pakistan as the country’s first denosumab biosimilar (120mg), and supply has now commenced. Mabwell has signed formal cooperation agreements for this product in 33 countries, including Brazil, Saudi Arabia, and Indonesia, and has submitted registration applications in 8 countries.

Denosumab, due to its demonstrated good therapeutic effects, has been recommended by multiple expert consensuses or treatment guidelines. As the first denosumab biosimilar (120mg) launched in China, MAIWEIJIAN possesses early-mover advantages. Compared with bisphosphonates commonly used in clinical treatment, denosumab has the following advantages:

Targeted action – It specifically binds to RANKL, blocking the RANKL/RANK/OPG signaling pathway, thereby preventing and treating SREs caused by bone metastases.
Superior clinical efficacy – It demonstrates significantly better clinical efficacy than bisphosphonates and remains effective in patients who have failed bisphosphonate therapy.
Favorable safety profile – It is not cleared by the kidneys, and patients receiving denosumab experience fewer renal toxicity side effects.
Previously, Mabwell published the Phase I and Phase III clinical study results of this product in International Immunopharmacology and the top-tier international journal JAMA Oncology, respectively. Through head-to-head pharmacokinetic comparisons and clinical efficacy studies in patients with bone metastases from solid tumors, the product has been systematically and comprehensively demonstrated to be similar to the reference product in terms of pharmacokinetics, pharmacodynamics, clinical efficacy, and safety.

(Press release, Mabwell Biotech, APR 15, 2026, View Source [SID1234664407])

On April 15, 2026 Arima Genomics, Inc., a company leveraging whole-genome sequence and structure information to advance cancer therapy selection, reported that it will present new data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17-22, 2026, in San Diego, California. The five presentations will highlight the power of Arima’s Hi-C sequencing-based approach to detect clinically relevant structural variants and uncover important drivers of cancer across solid tumors. Together, they reflect Arima’s vision for expanding cancer genomics beyond sequence alone.

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"Structural variants are an important driver of cancer biology, and Arima is focused on bringing that dimension into cancer genomics," said Anthony Schmitt, PhD, Senior Vice President of Science at Arima Genomics. "The data we will present at AACR (Free AACR Whitepaper) reflect the breadth of that opportunity across solid tumors."

The presentations include data demonstrating Arima’s ability to detect structural variants in lung and gastrointestinal tumors, showing concordance with traditional methods while also identifying variants those methods may miss. That capability, demonstrated across multiple studies, underpins Arima’s Aventa FusionPlus clinical assay. Additional presentations demonstrate the ability to detect and predict the functional impact of enhancer hijacking rearrangements and extrachromosomal DNA (ecDNA) amplifications in non-small cell lung cancer (NSCLC). A fifth presentation extends Arima’s work in fusion and rearrangement detection into gynecologic carcinosarcoma through analysis of aberrations involving genes potentially linked to homologous recombination deficiency (HRD). Together, the AACR (Free AACR Whitepaper) data show the range of biological and clinical questions that a structural variant-focused approach can address.

"These studies show how Arima’s technology provides a new lens with which to view the cancer genome in a way that no other technology can," said Tom Willis, PhD, Chief Executive Officer of Arima Genomics. "We are already putting this approach to work for patients through our Aventa clinical tests, while continuing to build the evidence and applications that support a more complete view of cancer."

List of Poster Presentations

April 20, 2026, 2:00-5:00 PM

Detection and functional assessment of extrachromosomal DNA amplifications in FFPE lung tumor specimens using Hi-C sequencing

Poster Number: 3259
Location: Section 22
Discovery and functional characterization of enhancer hijacking oncogene rearrangements in NSCLC using Hi-C sequencing of FFPE tumors

Poster Number: 3747
Location: Section 41
Fusions and rearrangement detection in gastrointestinal and lung tumors leveraging low-pass whole-genome sequencing based Hi-C chemistry

Poster Number: 3817
Location: Section 44
Genome wide testing of archived ovarian and uterine carcinosarcoma FFPE tissue using FusionPlus Hi-C to determine HRD status

Poster Number: 3970
Location: Section 49
April 21, 2026, 2:00-5:00 PM

Actionable fusions and rearrangements can be efficiently identified by Hi-C whole genome sequencing in lung tumors

Poster Number: 6521
Location: Section 43

(Press release, Arima Genomics, APR 15, 2026, View Source [SID1234664423])