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Natera Publishes Clinical Validation of Latitude™ Tissue-Free MRD Test in Colorectal Cancer

On January 21, 2026 Natera, Inc. (NASDAQ: NTRA), a global leader in cell-free DNA and precision medicine, reported the publication in npj Precision Oncology of the validation study for its Latitude tissue-free molecular residual disease assay (tfMRD) in colorectal cancer (CRC). The peer-reviewed publication builds upon data that was previously presented at the 2025 European Society for Medical Oncology GI Congress (ESMO GI).

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The study analyzed 1,230 timepoints from 195 CRC patients who participated in the GALAXY clinical trial, one of the largest and most comprehensive tfMRD studies in resectable CRC. The scale and rigor of this dataset, combined with excellent clinical performance, provides support for submission to the Centers for Medicare & Medicaid Services’ (CMS) Molecular Diagnostics Services Program (MolDX). Key findings from the publication include:

High sensitivity: longitudinal sensitivity of 84.4%, with median lead time of 4.6 months ahead of radiographic recurrence.
High specificity: 97.2% sample-level specificity and 92.1% patient-level specificity, providing strong actionability when an MRD-positive is observed.
Robust prognostic value: MRD-positivity was associated with worse outcomes in both the MRD (HR: 10, p<0.001) and surveillance settings (HR: 31.9, p<0.001).
Clear predictive value for adjuvant chemotherapy (ACT) benefit: In high-risk stage II and stage III patients, those who were MRD-positive following surgery experienced a significant benefit from ACT (adj.HR=0.014, P<0.0001), compared to MRD-negative patients, who observed no meaningful treatment benefit.
Latitude is a methylation-based test that detects circulating tumor DNA (ctDNA) without the need for tumor tissue. The assay complements Natera’s tumor-informed and personalized Signatera test, providing physicians and patients with a highly-sensitive testing option when tissue is unavailable. Natera is currently developing and validating Latitude for several additional cancer indications, expected to launch in 2026.

"The data from our latest publication underscores Natera’s commitment to providing solutions for patients diagnosed with colorectal cancer," said Minetta Liu, M.D., chief medical officer of oncology and early cancer detection at Natera. "Latitude delivers high-performance MRD detection for clinical situations where tumor-informed testing with Signatera is not possible or practical. Since launching in 2025, Latitude has experienced strong interest among clinicians, and we look forward to offering the test in additional histologies."

(Press release, Natera, JAN 21, 2026, View Source [SID1234662147])

Opna Bio Announces Orphan Drug Designation Granted to OPN-2853 (Zavabresib) for the Treatment of Myelofibrosis

On January 21, 2026 Opna Bio, a clinical-stage biopharmaceutical company focused on the discovery and development of novel oncology therapeutics, reported that OPN-2853, a bromodomain and extra-terminal motif (BET) small molecule inhibitor, has been granted Orphan Drug Designation (ODD) for the treatment of myelofibrosis (MF) by the U.S. Food and Drug Administration (FDA). Additionally, the generic name of zavabresib for OPN-2853 has been approved by the International Nonproprietary Names (INN) for Pharmaceutical Substances.

Myelofibrosis is a rare and serious type of blood cancer characterized by bone marrow scarring, which leads to ineffective blood cell production and symptoms such as severe fatigue, enlarged spleen, and anemia. Myelofibrosis affects approximately 25,000 people in the U.S.

"Receiving Orphan Drug Designation for zavabresib in myelofibrosis is a significant regulatory milestone for Opna Bio and highlights the urgent need for new and effective treatment options for patients with this disease," said Reinaldo Diaz, chief executive officer of Opna Bio. "Our investigator-sponsored clinical trial with zavabresib and ruxolitinib has shown impressive results to date, including durable spleen reduction in patients with advanced myelofibrosis. We believe that selective BET inhibition alongside JAK inhibition offers a promising new therapeutic approach for patients with myelofibrosis. We are further encouraged by recent positive meetings with the FDA to continue to test zavabresib in additional clinical studies."

The FDA grants Orphan Drug Designation to investigational therapies intended for the treatment, diagnosis or prevention of rare diseases that affect fewer than 200,000 people in the United States. The designation provides several benefits, including tax credits for clinical trial costs, a waiver of certain FDA fees, and eligibility for seven years of market exclusivity upon approval.

In the ongoing Phase 1 PROMise study led by Professor Adam Mead at the University of Oxford through a collaboration with Cancer Research UK (CRUK), zavabresib is being evaluated as an add-on to ruxolitinib in patients with myelofibrosis who are no longer responding to ruxolitinib alone. Data presented at the American Society of Hematology (ASH) (Free ASH Whitepaper) conference in December 2025 showed a 50% or greater reduction of spleen length in 16 of 26 evaluable patients on the combination treatment when compared to baseline.

(Press release, Opna Bio, JAN 21, 2026, View Source [SID1234662146])

NEOK Bio Receives FDA IND Approval for NEOK001, A First-In-Class B7-H3/ROR1 Bispecific ADC for Treatment of Solid Tumor Cancers

On January 21, 2026 NEOK Bio, Inc., an oncology therapeutics company focused on the development of novel antibody drug conjugates (ADCs) for improving outcomes for cancer patients, reported that the U.S. Food and Drug Administration (FDA) has approved the Company’s Investigational New Drug (IND) application for NEOK001, enabling initiation of a Phase 1 clinical trial.

NEOK001 is a bispecific ADC designed to target B7-H3 and ROR1, two surface proteins highly expressed in cancer cells. The therapy is conjugated with a topoisomerase I inhibitor payload via a linker. Preclinical NEOK001 studies have shown superior in vivo efficacy in solid tumors compared to traditional monovalent ADCs.

"We are thrilled to receive IND clearance for NEOK001, a milestone that allows NEOK Bio to advance this first-in-class bispecific ADC into clinical development. We look forward to studying its potential to address significant unmet needs for patients with cancers that co-express these targets," said Mayank Gandhi, CEO of NEOK Bio. "We anticipate dosing the first patient in the coming months and expect to share initial clinical data in 2027."

Backed by ABL Bio, a global leader in antibody engineering, NEOK Bio was launched last year to advance a pipeline of differentiated bispecific ADCs. NEOK001 is the first program to enter clinical development, representing the company’s commitment to advancing next-generation ADCs and positioning NEOK Bio as an emerging leader in ADC innovation in the U.S.

(Press release, Neok Bio, JAN 21, 2026, View Source [SID1234662145])

Infinitopes Expands Seed Financing to $35 Million to Accelerate Clinical Development of Precision Cancer Vaccine

On January 21, 2026 Infinitopes, a clinical-stage cancer vaccine biotechnology company, reported the successful completion of the second close of its seed financing round, securing an additional $15.4 million and bringing the total raised to $35.1 million. This latest investment was co-led by Octopus Ventures and new investor Amplify Bio, with further participation from new investor Macmillan Cancer Support alongside existing investors Cancer Research Horizons and Manta Ray Ventures.

This funding comes as the company launches its first-in-human, double-blind, randomised, placebo-controlled clinical trial of ITOP1, its leading precision therapeutic vaccine aimed at preventing recurrence in oesophageal cancer, an area where clinical need remains largely unmet. The Phase I/IIa VISTA trial is to be conducted across multiple UK NHS university cancer centres and firmly positions Infinitopes at the cutting edge of the sector.

Jonathan Kwok, Chief Executive Officer of Infinitopes, said: "I’m honoured to welcome leading US West Coast biofund Amplify Bio and ecosystem champions for better patient care, Macmillan, onto our cap table. This new funding unlocks our potentially groundbreaking Phase I/IIa trial, enabling proof-of-concept evaluation of Infinitopes’ AI/ML-precision targeted, off-the-shelf vaccine platform to prevent recurrence after surgical resection. We aim to lead the development of innovative medicines that bring hope to patients suffering from cancers with unmet medical needs. We anticipate sharing our early findings at major conferences later this year."

Elliot Hershberg, Partner at Amplify Bio, remarked: "Recent clinical evidence has made it abundantly clear that the time for cancer vaccines is now. After years of searching, Infinitopes has clearly distinguished itself as the company positioned to drive this progress forward. The combination of rigorous AI-powered immunomics profiling, a highly scalable off-the-shelf vector, and a defined clinical strategy is exactly what this field needs. Infinitopes has the potential to redefine immunotherapy and precision oncology in the years to come."

(Press release, Infinitopes, JAN 21, 2026, View Source [SID1234662143])

Kanazawa University research: Visualizing how cancer drugs reshape proteins linked to lung cancer

On January 21, 2026 Researchers at Nano Life Science Institute (WPI-NanoLSI) and the Cancer Research Institute at Kanazawa University reported how targeted lung cancer drugs alter the shape and behavior of a key cancer-driving protein—revealing a hidden mechanism that helps explain why some treatments stop working over time.

Targeted cancer therapies are designed to block specific molecules that drive tumor growth. One such molecule, ALK, plays a central role in a form of lung cancer caused by a genetic fusion known as EML4–ALK. Drugs that inhibit ALK have dramatically improved patient outcomes, but many patients eventually develop resistance, limiting long-term effectiveness.

Until now, it has been difficult to understand this resistance at a molecular level because large parts of the EML4–ALK protein are highly flexible and constantly changing shape, making them difficult to analyze using conventional structural biology techniques.

Watching cancer proteins move, one molecule at a time

In this study, Seijo Yano from the Nano Life Science Institute (WPI-NanoLSI) and colleagues at the Cancer Research Institute at Kanazawa University used high-speed atomic force microscopy (HS-AFM) to directly observe individual EML4–ALK proteins in real time.

This approach allowed the team to watch how the protein repeatedly assembles and disassembles into small clusters and how these movements change when cancer drugs are added. Among several variants of EML4–ALK, one clinically important form—known as variant 3—showed especially complex and unstable behavior.

The researchers discovered a previously unknown structural element within a flexible region of the protein that briefly forms a compact shape and strongly influences how the protein clusters. This structural feature was found in variant 3, which is known to respond less favorably to treatment in patients.

Cancer drugs reshape protein structure—and resistance blocks this effect

The study also revealed that commonly used ALK inhibitors do more than simply suppress enzyme activity. These drugs physically reshape the flexible regions of the protein, reducing its ability to form clusters that drive cancer signaling.

However, this structural effect was lost when the protein carried a well-known drug-resistance mutation (ALK G1202R), providing a direct structural explanation for why certain tumors become unresponsive to treatment.

"Our results show that ALK inhibitors work not only by blocking kinase activity, but also by altering the overall structure of the cancer-causing protein," says Yano, who led the study. "This long-range structural effect disappears in drug-resistant mutants, which may be one reason why resistance emerges in clinical settings."

Toward better strategies against drug resistance

By directly visualizing how cancer drugs alter protein structure at the single-molecule level, this research provides new insight into why different patients respond differently to the same therapy. The findings suggest that future drug development could benefit from targeting not only enzyme activity, but also the structural dynamics of oncogenic fusion proteins.

This work highlights the unique power of high-speed AFM to reveal molecular behaviors that are otherwise inaccessible and opens new avenues for designing next-generation therapies for ALK-driven lung cancer.

(Press release, Kanazawa University, JAN 21, 2026, View Source [SID1234662142])