Terremoto Biosciences Closes $108 Million Series C Financing to Advance Selective AKT1-Inhibitors in Oncology and Hereditary Hemorrhagic Telangiectasia

On April 15, 2026 Terremoto Biosciences, a biotechnology company developing highly targeted, small molecule medicines, reported the closing of a $108 million Series C financing round. The round includes new investors RA Capital Management, Deep Track Capital, Osage University Partners (OUP), and BeOne Medicines, and participation from existing investors OrbiMed, Third Rock Ventures, Novo Holdings, and Cormorant Asset Management.

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"Proceeds from this financing enable us to advance our lead AKT1-selective inhibitor programs through Phase 1 clinical development for patients with cancer and rare diseases such as hereditary hemorrhagic telangiectasia," said Charles Baum, M.D., Ph.D., Chief Executive Officer of Terremoto. "We are grateful for the support from new and existing investors as we work to unlock the full potential of selective AKT1 inhibition and bring more effective and better tolerated treatment options to patients with significant unmet need."

Terremoto’s lead oncology program, TER-2013, is currently in Phase 1 clinical development for solid tumors harboring genetic alterations in PIK3CA, AKT, or PTEN, which are implicated in a significant proportion of cancers, including more than half of patients with HR-positive breast cancer. The company is also advancing TER-4480, a program targeting hereditary hemorrhagic telangiectasia (HHT), a rare, inherited bleeding disorder characterized by abnormal blood vessel formation and significant morbidity, with currently no approved therapies. TER-4480 is expected to enter the clinic later this year.

AKT is a key regulatory protein implicated in driving disease progression in both cancer and HHT. Among the three structurally similar isoforms (AKT1, AKT2, AKT3), AKT1 has been shown in preclinical studies to be the predominant disease driver, while AKT2 is linked to adverse effects such as rash and dysregulation of glucose homeostasis. While there has been considerable advancement of other PI3K/AKT pathway inhibitors, the efficacy of these treatments has often been limited by toxicities – primarily due to PI3Kα or AKT2 inhibition. Using advanced medicinal chemistry capabilities, Terremoto has developed a novel class of AKT1-selective inhibitors to overcome these limitations, aiming to achieve deeper and more durable treatment response with an improved tolerability profile.

(Press release, Terremoto Biosciences, APR 15, 2026, View Source [SID1234664404])

Quantum-Si Announces Two Customer Posters to be Presented at the American Association of Cancer Research Annual Meeting

On April 15, 2026 Quantum-Si Incorporated (Nasdaq: QSI) ("Quantum-Si," "QSI" or the "Company"), a proteomics company redefining protein analysis through single-molecule protein sequencing, reported that there will be two customer posters presented at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) annual meeting on April 17-22, 2026 in San Diego, California.

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Poster 2421; April 20, 2026
Primary Author: Nigel O’Neil, PhD
Poster Title: Combining deep mutational scanning and next-generation protein sequencing to harness dominant protein variants to develop DNA repair inhibitors

In the first poster, the researchers describe a complementary genetic (high throughput screens) and proteomic (benchtop protein sequencing) approach to find and model the behavior of therapeutics targeting DNA repair enzymes.

Poster 7650; April 22, 2026
Primary Author: Gloria Sheynkman, PhD
Poster Title: High-resolution detection of post-translational modifications using single-molecule protein sequencing

In the second poster, the researchers demonstrated the ability to resolve and quantify multiple PTMs using Quantum-Si’s single-molecule protein sequencing technology. The authors suggested that the technology could be used to add proteoform characterization to biomarker studies, providing additional resolution not readily available in broad biomarker screening panels. The authors further concluded that they expect this technology could democratize advanced protein characterization, making the high-resolution detection of PTMs available to a broader scientific community.

"We are excited to see new customer data being presented at key industry conferences like AACR (Free AACR Whitepaper), that continue to demonstrate the power of our proprietary single-molecule protein sequencing technology," said Jeff Hawkins, President and Chief Executive Officer of Quantum-Si. "We invested significant effort during 2025 to build a pipeline of studies that would demonstrate the power of our technology, and we are very pleased to have a steady flow of customer pre-prints, publications and posters being released this year as we work to expand awareness and build momentum towards the launch of Proteus."

(Press release, Quantum SI, APR 15, 2026, View Source [SID1234664420])

Knight to Present at the 2026 Bloom Burton & Co. Healthcare Investor Conference

On April 15, 2026 Knight Therapeutics Inc. (TSX: GUD) ("Knight"), a pan-American (ex-US) specialty pharmaceutical company, reported that Samira Sakhia, President and Chief Executive Officer, is scheduled to present a corporate update at the 2026 Bloom Burton & Co. Healthcare Investor Conference on Tuesday, April 21, 2026, at 2:00 p.m. ET at the Metro Toronto Convention Centre (North Building) in Toronto. A copy of the presentation will be available at www.knighttx.com.

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(Press release, Knight Therapeutics, APR 15, 2026, View Source;Co–Healthcare-Investor-Conference/default.aspx [SID1234664405])

TRIANA Biomedicines Announces Oral Presentation of TRI-611 and Additional Poster Presentations at the American Association for Cancer Research Annual Meeting 2026

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])

NMPA Accepts IND Application for Mabwell’s Innovative LILRB4/CD3 TCE Bispecific Antibody 6MW5311

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])