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.

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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])

On January 21, 2026 Autolus Limited, a wholly owned subsidiary of Autolus Therapeutics plc (the "registrant", and together with Autolus Limited, the "Company"), reported to have entered into a Master Service Agreement with AGC Biologics S.p.A ("AGC") for the manufacture and supply of lentiviral vector (the "Agreement"), a raw material which is critical for the Company’s manufacture of CAR-T products for clinical and commercial use. The Agreement replaces and supersedes the prior arrangement between the Company and AGC, pursuant to which AGC has provided similar products and services.

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The Agreement sets forth the general terms and conditions applicable to AGC’s provision of products and services to the Company; specific projects will be set forth in individual work orders executed separately by the parties. The Agreement contains customary provisions regarding order placement and fulfillment, governance, regulatory support, change management, risk allocation, intellectual property, and confidentiality. The Agreement runs for a fixed term of ten years, and may be terminated by either party for default, or by the Company upon written notice (subject, in the latter case, to the payment of certain fees by the Company). The Agreement is non-exclusive with respect to each party. However, under the Agreement and the initial statement of work thereunder, the Company has committed to purchase a minimum of 14 batches of lentiviral vector during the first two calendar years of the term, and to purchase a minimum value of EUR 25 million of products and services during the subsequent five-year period. The Agreement also provides AGC with the first right to negotiate with the Company regarding the provision of new manufacturing activities in relation to the Company’s obecabtagene autoleucel, or obe-cel, product.

The foregoing summary of the material terms of the Master Service Agreement does not purport to be complete and is qualified in its entirety by reference to such Master Service Agreement, which will be filed as an exhibit to the Company’s Quarterly Report on Form 10-Q for the quarter ending March 31, 2026. Portions of the Agreement may be omitted pursuant to Item 601(b)(10)(iv) or Item 601(a)(5) of Regulation S-K under the Securities Exchange Act of 1934, as amended.

(Filing, 8-K, Autolus, JAN 21, 2026, View Source [SID1234662203])

On January 21, 2026 BioNTech SE (Nasdaq: BNTX, "BioNTech" or "the Company") reported that the U.S. Food and Drug Administration ("FDA") has granted Fast Track designation to BNT113, an investigational mRNA cancer immunotherapy, for the treatment of patients with human papillomavirus type 16 positive ("HPV16+") head and neck squamous cell carcinoma ("HNSCC") expressing PD-L1, a distinct cancer type associated by infection with high-risk human papillomavirus.

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The FDA Fast Track process is designed to facilitate the development and expedite the review of new drugs and vaccines that are intended to treat or prevent serious conditions and have the potential to address an unmet medical need. The designation has been granted based on preliminary safety and efficacy data from the ongoing pivotal Phase 2/3 AHEAD-MERIT clinical trial (NCT04534205) evaluating BNT113 in combination with pembrolizumab versus pembrolizumab monotherapy as a first-line treatment in patients with unresectable recurrent or metastatic HPV16+ HNSCC expressing PD-L1.

HNSCC is the seventh most common cancer type worldwide with increasing global incidence, mainly driven by a rise in HPV16-related oropharyngeal tumors, the most common subtype of HNSCC.2,4 About one third of HNSCC cases are HPV-positive following a HPV infection, with a rising trend, of which about 90% of oropharyngeal cancers are driven by the subtype HPV16.1,5 Despite the distinct characteristics of HPV-positive tumors, there are currently no HPV-targeted treatments approved.3 Many patients with HPV16+ HNSCC experience disease progression under current standard of care treatments with a median overall survival of 20.7 months6, underlining the unmet medical need for novel HPV-targeted chemotherapy-free treatment options that improve long-term survival. HNSCC is among BioNTech’s key tumor areas.

BNT113 is an investigational mRNA cancer immunotherapy encoding the E6 and E7 proteins of HPV16, that are frequently found in HPV16+ solid tumors. This mRNA cancer immunotherapy approach is designed to induce HPV16-specific anti-tumor immune responses, thereby aiming to enhance clinical responses in patients being treated with checkpoint inhibitor standard of care treatment.

(Press release, BioNTech, JAN 21, 2026, View Source [SID1234662126])

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.

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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])

On January 21, 2025 Breakpoint Therapeutics GmbH ("Breakpoint"), a company dedicated to the discovery and development of drugs targeting the DNA Damage Response (DDR), reported that it will present preclinical data from its polymerase theta (Pol θ / POLQ) inhibitor programme in an oral presentation at the DDR Inhibitors Summit, being held January 27-29, 2026 in Boston (MA), USA.

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DNA polymerase theta is a DNA repair enzyme that is largely absent in normal cells but displays aberrant expression in multiple cancer types which often correlates with poor prognosis. Inhibition of Pol θ is a validated therapeutic modality in certain tumour-specific contexts.

Details of the presentation are as follows:

Title: Targeting Polθ’s Dual Domains to Guide Candidate Selection & Strategic Partnering

Date: Wednesday, 28 January, 2026

Time: 11:00 – 11:30 a.m. ET

In addition, Jon will participate in a panel discussion on the topic of "Uniting Founders and Funders to Align Scientific Vision with Investment Strategy" scheduled for Thursday, 29 January, 2026 at 8:30am.

(Press release, Breakpoint Therapeutics, JAN 21, 2026, View Source [SID1234662127])