On March 17, 2026 Cancer Research UK’s Centre for Drug Development (CDD) and NovalGen reported that the first patient has been dosed in a Phase 1 clinical trial evaluating NVG‑222, NovalGen’s next-generation self‑regulating T‑cell engager for the treatment of ROR1‑positive blood cancers.

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NVG‑222 is a bispecific T‑cell engager targeting ROR1 and CD3 and is the first therapeutic candidate to use NovalGen’s proprietary AutoRegulation technology, a key innovation designed to mitigate excessive immune activation and cytokine-mediated toxicities, while maintaining sustained T-cell function and reducing exhaustion associated with continuous stimulation.

The trial is sponsored and delivered by Cancer Research UK’s Centre for Drug Development and is led by Chief Investigator Will Townsend at University College London Hospitals NHS Foundation Trust (UCLH), where the first patient received treatment. Cancer Research Horizons is managing the commercial partnership between NovalGen and Cancer Research UK.

The study is enrolling patients across the UK with ROR1‑positive blood cancers and uses an adaptive design to optimise dose, treatment and biomarker strategies. Dosing of the first patient marks an important step in translating AutoRegulated immune therapies from the laboratory into clinical testing.

Dr Lars Erwig, Director of the Centre for Drug Development at Cancer Research UK, said:

"Dosing the first patient is an important milestone for our collaboration with NovalGen. NVG‑222 reflects the kind of innovative, safety‑focused immunotherapy we aim to advance, and we’re proud to help bring this next‑generation treatment into the clinic."

Professor Amit Nathwani, Founder and CEO of NovalGen, said:

"The start of this Phase 1 trial is a defining moment for NovalGen and the patients we serve. With support from CRUK, we are moving towards a future of ‘intelligent’ biologics. Our AutoRegulation (AR) technology is designed to sense and respond to the biological environment in real-time, aiming to overcome the toxicity and

exhaustion hurdles that have historically limited T-cell based immunotherapies. NVG-222 marks the beginning of our mission to set a new standard for precision, potency and safety in next-generation immunotherapy."

Dr William Townsend, Consultant Haematologist at University College London Hospitals NHS Foundation Trust, said:

"This represents the start of the next chapter in the story of T-cell engaging strategies to treat blood cancers. It is exciting to be part of this Phase 1 clinical trial which shows the best of UK research and clinical trial delivery. I hope it will translate into tangible benefits for our patients."

(Press release, NovalGen, MAR 17, 2026, View Source [SID1234663625])

On March 17, 2026 Revolution Medicines, Inc. (Nasdaq:RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, reported that nine oral and poster presentations highlighting advances across its RAS(ON) inhibitor pipeline will be featured at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17–22, 2026 in San Diego.

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The presentations will include new Phase 1 data for zoldonrasib, a RAS(ON) G12D-selective inhibitor, in patients with previously treated KRAS G12D mutant non-small cell lung cancer, which will be featured in a plenary session.

The company will also present two Phase 1/2 datasets evaluating daraxonrasib, a RAS(ON) multi-selective inhibitor, in patients with first line metastatic pancreatic ductal adenocarcinoma (PDAC), including monotherapy data and daraxonrasib plus chemotherapy combination data, the latter of which will be featured in a mini-symposium session.

Additional presentations will highlight preclinical research supporting a new class of mutant-targeted catalytic RAS(ON) inhibitors, designed to maintain antitumor activity in the setting of emergent resistance.

Together, these presentations reflect the breadth of Revolution Medicines’ RAS(ON)-focused development strategy, spanning clinical studies across multiple tumor types and ongoing discovery efforts to address resistance and expand therapeutic opportunities for patients with RAS-driven cancers.

Details of the presentations are listed below.

Revolution Medicines Invited Presentation:

Title: Targeting the Oncogenic State of RAS: Lessons from Tri-Complex Inhibitors
Presenter: Mallika Singh, Ph.D., Revolution Medicines
Session: How KRAS Inhibitors Got to the Clinic: From Discovery to Patient Benefit
Date/Time: April 18; 3:00 p.m. – 3:20 p.m. PST

Revolution Medicines Oral Presentation:

Title: Preliminary Safety and Clinical Activity of Zoldonrasib (RMC-9805), an Oral, RAS(ON) G12D-Selective, Tri-Complex Inhibitor in Patients with Previously Treated KRAS G12D Non-Small Cell Lung Cancer (NSCLC)
Presenter: Jonathan Reiss, M.D., UC Davis Comprehensive Cancer Center
Abstract
Number: CT021
Session: New Frontiers in Precision Oncology
Date/Time: April 19; 1:30 p.m. – 1:45 p.m. PST

Revolution Medicines Mini Symposiums:

Title: Daraxonrasib plus Chemotherapy as First Line Treatment for Patients with Metastatic Pancreatic Adenocarcinoma (mPDAC)
Presenter: Brian Wolpin, M.D., Dana-Farber Cancer Institute
Abstract
Number: LB407
Session: Late-Breaking Research
Date/Time: April 21; 4:05 p.m. – 4:20 p.m. PST

Title: Discovery of a New Class of Mutant-Targeted Catalytic RAS(ON) Inhibitors with Retained Antitumor Activity in Setting of Emergent Resistance Due to Elevated RAS Flux
Presenter: Jacqueline (Jan) Smith, Ph.D., Revolution Medicines
Abstract
Number: 6782
Session: Targeted Protein Degradation and Non-canonical Oncogenic Signaling
Date/Time: April 21; 4:05 p.m. – 4:20 p.m. PST

Revolution Medicines Posters:

Title: RAS(ON) Inhibition in both Cancer and Immune Cells by Daraxonrasib Drives Antitumor Immunity
Presenter: Nataliya Shifrin, Ph.D., Revolution Medicines
Abstract
Number: 2831
Session: Immune Mechanisms Invoked by Other Therapies and Exposures
Date/Time: April 20; 2:00 p.m. – 5:00 p.m. PST

Title: RASolve 301: A Phase 3 Study of Daraxonrasib (RMC-6236) vs. Docetaxel in Patients with Previously Treated RAS-mutant NSCLC
Presenter: Ferdinandos Skoulidis, M.D., Ph.D., MRCP, MD Anderson Cancer Center
Abstract
Number: CT215
Session: Late-Breaking Research
Date/Time: April 21; 9:00 a.m. – 12:00 p.m. PST

Title: Daraxonrasib Monotherapy as First Line Treatment for Patients with Metastatic Pancreatic Adenocarcinoma
Presenter: Eileen O’Reilly, M.D., Memorial Sloan Kettering Cancer Center
Abstract
Number: LB337
Session: Late-Breaking Research: Clinical Research 3
Date/Time: April 21; 2:00 p.m. – 5:00 p.m. PST

Title: RAS(ON) Multi-Selective Inhibitors Stimulate the Hydrolysis of RAS-GTP to RAS-GDP and Drive Synergistic Combination Benefit with KRAS(OFF) Inhibitors in G12 Mutant Tumors
Presenter: Kyle Seamon, Ph.D., Revolution Medicines
Abstract
Number: 5696
Session: Mechanisms of Anticancer Drug Action
Date/Time: April 21; 2:00 p.m. – 5:00 p.m. PST

Collaborator Mini Symposium:

Title: Active RAS Inhibition Intercepts Pancreas Cancer in Mice
Presenter: Ben Stanger, M.D., Ph.D., Penn Pancreatic Cancer Research Center
Abstract
Number: LB406
Session: Late-Breaking Research
Date/Time: April 21; 3:50 p.m. – 4:05 p.m. PST

(Press release, Revolution Medicines, MAR 17, 2026, View Source [SID1234663624])

On March 17, 2026 Outrun Therapeutics ("Outrun" or "the Company"), a biotech developing protein stabilising therapeutics identified by its proprietary XL discovery platform, reported the selection of its lead programme for the treatment of HPV positive head and neck cancer. It also announced the formation of its Scientific Advisory Board comprising world-class experts in E3 ligase biology and head and neck cancer.

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Outrun has selected an E6AP inhibitor strategy as the lead programme from its first-in-class therapeutic pipeline developed through the application of its proprietary XL discovery platform. This platform has been used to profile over 45 diverse E3 ligases across a wide range of indications in oncology, neurology, cardiovascular and auto-immune diseases. The Company expects to announce a development candidate later this year.

E6AP is an E3 ubiquitin ligase that regulates the expression of a key tumour suppressor protein in HPV positive cancers, such as head and neck cancer. Inhibiting this enzyme represents a first-in-class strategy to directly stabilise tumour suppressor protein levels, paving the way to a meaningful impact on patients’ lives. HPV positive cancers account for around 4.5% of cancers worldwide, with the global market size expected to exceed $14 billion by 2031.

To help drive the advancement of the programme and the Company’s wider pipeline of first-in-class small molecule E3 ligase inhibitors, Outrun has appointed leading experts Glenn Hanna, Kevin Harrington, Gigi Lozano, Donald Ogilvie, and Martin Scheffner to its SAB. They join Outrun’s Founder, Non-executive Director, and Chair of the SAB, Professor Satpal Virdee.

These international experts bring extensive expertise in E3 ligase biology and head and neck cancer and will provide critical translational insights as Outrun advances its lead programme towards the clinic.

Dr Tony Johnson, Board Chair and Interim CEO of Outrun Therapeutics, said: "Outrun’s mission is to develop protein stabilising therapeutics to treat disease, and the selection of our lead programme, for the treatment of HPV positive head and neck cancer, is an important milestone in our journey. This is a massively underserved patient population, and we are confident that our novel approach to protein stabilisation offers a breakthrough route to bringing meaningful treatments to those in need."

Professor Satpal Virdee, Founder, Non-executive Director, and Chair of the SAB at Outrun Therapeutics, added: "Attracting such high-profile and experienced figures to our SAB is tremendous validation of the novel nature of our technology, and we are grateful for their commitment. Their expertise will be invaluable as we develop the translational strategy, clinical design, and biomarker validation to support our goal of establishing efficacy and differentiation in the HPV-induced head and neck cancer field, and transition to a clinical stage company."

(Press release, Outrun Therapeutics, MAR 17, 2026, View Source [SID1234663623])

On March 17, 2026 ORIC Pharmaceuticals, Inc. (Nasdaq: ORIC), a clinical stage oncology company focused on developing treatments that address mechanisms of therapeutic resistance, reported that multiple abstracts highlighting the potential of rinzimetostat (ORIC-944), a potent and selective allosteric inhibitor of PRC2 to treat prostate cancer, have been accepted for poster presentations at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place April 17-22, 2026 in San Diego, CA. All regular abstracts are available for viewing via AACR (Free AACR Whitepaper)’s online itinerary planner located here.

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Poster presentations details:

Date & Time: Wednesday, April 22, 2026, 9:00 a.m. – 12:00 p.m. PT
Session Category: Experimental and Molecular Therapeutics
Session Title: Novel Strategies to Reverse Drug Resistance
Location: Poster Section 14

Title: Rinzimetostat, an allosteric EED inhibitor with best-in-class properties for the treatment of prostate cancer, is effective in PRC2 methyltransferase-resistant settings in preclinical studies
Abstract Number: 7120
Poster Number: Board Number 9

Abstract Highlights
Rinzimetostat is a potent and highly selective next-generation allosteric PRC2 inhibitor targeting the EED subunit that has demonstrated potential best-in-class efficacy and safety in a dose exploration trial in combination with androgen receptor (AR) inhibitors. To further evaluate the possible benefits of inhibiting PRC2 activity through EED targeting, preclinical studies investigated rinzimetostat versus EZH2- or EZH1/2-targeting agents in the context of proposed acquired resistance mechanisms. Biochemical assays demonstrated that rinzimetostat maintained potent inhibition of PRC2 complexes containing either EZH1 or EZH2 as the enzymatic subunit, while EZH2 or EZH1/2 dual inhibitors showed reduced activity in EZH1-containing complexes. Consistent with the biochemical data, rinzimetostat retained antitumor activity in prostate cancer cells overexpressing EZH1, while EZH2 inhibitors mevrometostat and tazemetostat lost potency in this context. Rinzimetostat also maintained inhibition of H3K27me3 in prostate cancer cells expressing the clinically reported EZH2-inhibitor acquired resistance mutation EZH2 Y666N, while EZH2 inhibitors did not reduce H3K27me3. In addition, in prostate cancer cells expressing the acquired resistance mutation EED-H213R, which is associated with clinical resistance to dual EZH1/2 inhibition, rinzimetostat equally inhibited H3K27me3 in both mutant and wild-type settings, while an EZH1/2 inhibitor did not. Together, these data suggest that rinzimetostat, as an EED inhibitor, has the potential for superiority in resistance context of EZH1 overexpression, as well as in acquired resistance mutant contexts of EZH2 and EZH1/2 inhibitors. A global phase 1b trial of rinzimetostat in combination with AR inhibitors is ongoing in metastatic prostate cancer (NCT05413421).

Title: Rinzimetostat blockade of PRC2 activity, a key mechanism of treatment resistance, improves response of androgen receptor pathway inhibition across a spectrum of prostate cancer models
Abstract Number: 7132
Poster Number: Board Number 21

Abstract Highlights
Rinzimetostat is a potent and highly selective next-generation allosteric PRC2 inhibitor targeting the EED subunit that has demonstrated potential best-in-class efficacy and safety in a dose exploration trial in combination with AR inhibitors. Transcriptome analyses of more than 1,000 prostate cancer patient samples spanning primary prostate cancer, metastatic castration-resistant prostate cancer (mCRPC), and neuroendocrine prostate cancer (NEPC) revealed gene expression patterns driving prostate cancer progression. Pseudotime analysis of tumor transcriptomes highlighted the eventual reduction in AR expression, AR signaling and luminal identity during mCRPC that may reflect lineage plasticity and cell state reprogramming. Integrated analysis across treatment lines identified epigenetic regulators, including PRC2, whose activity signatures increase during disease progression and may contribute to tumor heterogeneity and resistance to androgen receptor pathway inhibitors (ARPIs), further supporting the rationale for PRC2 inhibition. Rinzimetostat in combination with the AR inhibitor darolutamide demonstrated antitumor activity across a broad spectrum of in vivo prostate cancer models representing the treatment continuum, including castration-sensitive and castration-resistant disease, ARPI-sensitive and ARPI-resistant settings, and tumors harboring both AR-mutant and AR wild-type backgrounds. Together, these findings suggest that targeting PRC2 with rinzimetostat re-sensitizes ARPI-resistant tumors to AR pathway inhibition and blocks prostate tumor adaptation. A global phase 1b trial of rinzimetostat in combination with AR inhibitors is ongoing in metastatic prostate cancer (NCT05413421).

(Press release, ORIC Pharmaceuticals, MAR 17, 2026, View Source [SID1234663622])

On March 17, 2026 One-carbon Therapeutics, a clinical-stage oncology company pioneering first-in-class targeted therapies based on deep understanding into cancer biology, reported a strategic collaboration with Tempus AI Inc. (NASDAQ: TEM), a technology company leading the adoption of AI to advance precision medicine. The collaboration will leverage Tempus’ proprietary, de-identified multimodal database and bioinformatics expertise to advance molecular insights supporting the clinical development of TH9619.

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Through this collaboration, One-carbon Therapeutics will utilize Tempus’ analytical services to characterize the expression landscape across prioritized solid tumor indications. By integrating RNA sequencing data with clinical variables, the teams aim to uncover deep molecular insights that will inform the development of TH9619.

"Understanding the molecular dynamics of one-carbon metabolism across tumor types and treatment settings is fundamental to advancing TH9619 with precision," said Ana Slipicevic, Chief Executive Officer at One-carbon Therapeutics. "Tempus’ depth of molecular data and analytical rigor enables us to generate statistically robust evidence that can potentially guide clinical decision making and optimize development."

"At Tempus, our goal is to accelerate progress in oncology by translating complex molecular insights into meaningful therapeutic advances," said Ezra Cohen, MD, Chief Medical Officer, Oncology, at Tempus. "Through comprehensive analysis of our multimodal dataset, we are supporting One-carbon Therapeutics in characterizing the metabolic signatures across diverse tumor types. These insights are essential to informing research strategies and advancing the development of next-generation targeted cancer therapies."

By deepening the understanding of the biological mechanisms and genetic profiles associated with one-carbon metabolism across tumor types, the collaboration will strengthen the precision-driven clinical strategy for TH9619. Building on a deep understanding of how cancer cells depend on this pathway, these analyses may help identify patient populations most likely to benefit from treatment. This approach has the potential to enhance development efficiency, reduce uncertainty and ultimately help ensure that innovative targeted therapies reach the patients who need them most.

(Press release, One-carbon Therapeutics, MAR 17, 2026, View Source [SID1234663621])