On April 15, 2026 Zephyr AI, Inc. ("Zephyr AI"), a leader in precision medicine harnessing artificial intelligence to accelerate drug development, reported its schedule of research presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting in San Diego, California, April 17-22, 2026.

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The company’s posters will be presented by senior researchers and highlight novel work Zephyr AI is advancing with its biopharmaceutical and life science partners. The presentations feature multimodal AI approaches for predicting response to targeted therapies in patients with cancer, as well as checkpoint inhibitor response in patients receiving combination treatment. Across these investigations, Zephyr’s AI models operate on clinically available inputs—including liquid biopsy DNA, tissue-based molecular data, and whole-slide images—to generate drug response predictions and biological insights into tumor-intrinsic and tumor microenvironment features associated with treatment response.

"We are thrilled to showcase Zephyr AI’s work at this year’s AACR (Free AACR Whitepaper) meeting," said Zephyr AI CEO Allen Chao, PhD. "The utilization of AI with multimodal data and clinically available inputs is transforming research and accelerating discovery. This is a wonderful opportunity to share how our novel approach is helping drive important advances in cancer treatment."

Official schedule of Zephyr AI presentations at AACR (Free AACR Whitepaper):

Real world prediction and biological characterization of sotorasib sensitivity using multimodal AI and liquid biopsy genomic inputs (Presentation 5235)

Session Title: Biomarkers Predictive of Therapeutic Benefit 5
Presenter: Emily Vucic, VP Science
Session Date & Time: April 21, 9:00AM – 12:00PM
Location: Poster Section 42
Poster Board Number: 1

Multimodal AI predicts immune checkpoint inhibitor response from clinically available inputs and whole-slide images with explainable tumor biology and combination therapy insights (Presentation 1014)

Session Title: Biomarkers Predictive of Therapeutic Benefit 1
Presenter: Maayan Baron, Assoc Dir of Computational Biology
Session Date & Time: April 19, 2026 2:00PM – 5:00PM
Location: Poster Section 40
Poster Board Number: 8

Leadership from Zephyr AI will be attending AACR (Free AACR Whitepaper). Please contact [email protected] to request a meeting.

(Press release, Zephyr AI, APR 15, 2026, View Source [SID1234664419])

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])

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])

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])

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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Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

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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])