On December 22, 2025 Astrazeneca reported The LATIFY Phase III trial of ceralasertib in combination with Imfinzi (durvalumab) did not meet the primary endpoint of overall survival (OS) versus standard-of-care docetaxel in patients with locally advanced or metastatic non-small cell lung cancer (NSCLC). The trial evaluated patients without actionable genomic alterations (AGAs) whose disease progressed on or after prior immunotherapy and platinum-based chemotherapy.

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Susan Galbraith, Executive Vice President, Oncology Haematology R&D, AstraZeneca, said: "Our goal in the LATIFY trial was to reinvigorate the immune response of patients with lung cancer whose tumours stopped responding to available therapies by combining ATR inhibition with immunotherapy. While we are disappointed by this result, we remain committed to pioneering new medicines to address the urgent need to improve outcomes for patients with lung cancer through our industry-leading portfolio."

The combination of ceralasertib and Imfinzi was generally well tolerated, and the safety profile was consistent with the known profiles of each individual medicine, with no new safety concerns identified. These data will be presented at a forthcoming medical meeting.

Notes

NSCLC
Lung cancer is the leading cause of cancer death among both men and women, accounting for about one-fifth of all cancer deaths.1 Lung cancer is broadly split into small cell lung cancer (SCLC) or NSCLC, the latter accounting for about 80-85% of cases.2-3 Patients are most commonly diagnosed with metastatic disease, when the tumour has spread outside the lung.4 Approximately 12% of people with metastatic NSCLC will still be alive five years after diagnosis.5

LATIFY
LATIFY is a randomised, open-label, multi-centre, global Phase III trial of ceralasertib plus Imfinzi in patients with locally advanced or metastatic NSCLC without AGAs, and whose disease has progressed on or after prior anti-PD-(L)1 therapy and platinum-based chemotherapy. Patients were randomised 1:1 to receive ceralasertib 240mg twice daily oral tablets for seven days in combination with a 1,500mg fixed dose of Imfinzi on day eight every four weeks or docetaxel every three weeks until disease progression, unacceptable toxicity, withdrawal of consent or a discontinuation criterion was met.

The trial enrolled 594 patients across more than 20 countries. The primary endpoint is OS and secondary endpoints include progression-free survival, objective response rate, duration of response, time to response, disease control rate and patient reported outcomes.

Ceralasertib
Ceralasertib is an oral, potent and selective inhibitor of the ATR kinase, which is crucial for DNA damage responses and cell survival. Ceralasertib acts on the tumour microenvironment, moving it from a suppressed immune state into an activated state when combined with immunotherapy.

Imfinzi
Imfinzi (durvalumab) is a human monoclonal antibody that binds to the PD-L1 protein and blocks the interaction of PD-L1 with the PD-1 and CD80 proteins, countering the tumour’s immune-evading tactics and releasing the inhibition of immune responses.

In lung cancer, Imfinzi is the global standard of care based on OS in the curative-intent setting of unresectable, Stage III NSCLC in patients whose disease has not progressed after chemoradiotherapy (CRT). Additionally, Imfinzi is approved as a perioperative treatment in combination with neoadjuvant chemotherapy in resectable NSCLC, and in combination with a short course of Imjudo (tremelimumab) and chemotherapy for the treatment of metastatic NSCLC. Imfinzi is also approved for limited-stage SCLC in patients whose disease has not progressed following concurrent platinum-based CRT; and in combination with chemotherapy for the treatment of extensive-stage SCLC.

In addition to its indications in lung cancers, Imfinzi is also approved in combination with chemotherapy in locally advanced or metastatic biliary tract cancer and in combination with Imjudo in unresectable hepatocellular carcinoma (HCC). Imfinzi is also approved as a monotherapy in unresectable HCC in Japan and the European Union (EU), and in resectable, early-stage and locally advanced gastric and gastroesophageal junction cancers in the US.

Perioperative Imfinzi in combination with neoadjuvant chemotherapy is approved for muscle-invasive bladder cancer. In May 2025, Imfinzi added to Bacillus Calmette-Guérin induction and maintenance therapy met the primary endpoint of disease-free survival for patients with high-risk non-muscle-invasive bladder cancer in the POTOMAC Phase III trial.

Imfinzi in combination with chemotherapy followed by Imfinzi monotherapy is approved as a 1st-line treatment for primary advanced or recurrent endometrial cancer (mismatch repair deficient disease only in the US and EU). Imfinzi in combination with chemotherapy followed by Lynparza (olaparib) and Imfinzi is approved for patients with mismatch repair proficient advanced or recurrent endometrial cancer in the EU and Japan.

Since the first approval in May 2017, more than 414,000 patients have been treated with Imfinzi. As part of a broad development programme, Imfinzi is being tested as a single treatment and in combinations with other anti-cancer treatments for patients with NSCLC, bladder cancer, breast cancer, ovarian cancer and several gastrointestinal cancers.

(Press release, AstraZeneca, DEC 22, 2025, View Source [SID1234661585])

On December 22, 2025 Vividion Therapeutics, Inc. (Vividion), a clinical-stage biopharmaceutical company, and a wholly owned and independently operated subsidiary of Bayer AG, reported the publication of a manuscript describing the discovery and preclinical characterization of small molecules that activate KEAP1 via a novel covalent allosteric molecular glue mechanism to drive degradation of NRF2.

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The article, "A covalent allosteric molecular glue suppresses NRF2-dependent cancer growth" (Roy et al., Cancer Discov.), establishes NRF2 degradation via KEAP1 activation as a promising therapeutic approach for NRF2-activated cancers, including non-small cell lung cancer, esophageal squamous cell carcinoma, and head and neck squamous cell carcinoma.

"NRF2 has long stood as a symbol of undruggable cancer biology. Our team has opened a new chapter in targeting this critical cancer pathway through the discovery of KEAP1 activators," said Aleksandra Rizo, M.D., Ph.D., President and Chief Executive Officer of Vividion. "This research reflects the power of our platform to reveal unexpected allosteric mechanisms that could directly contribute to improved therapeutic efficacy, and ultimately better patient outcomes, for people with hard-to-treat cancers."

NRF2 is a transcription factor that promotes tumor growth, immune suppression, and resistance to cancer therapies. However, despite its clear role in disease progression, NRF2 has resisted direct pharmacologic inhibition due to its lack of canonical small-molecule binding pockets. Using Vividion’s covalent-first chemoproteomics platform, researchers discovered electrophilic small molecules that covalently bind to a specific cysteine residue on KEAP1 (C151) and induce an allosteric conformational change that enhances KEAP1’s interaction with the CUL3 E3 ligase complex. This stabilization of the KEAP1-CUL3 complex restores KEAP1’s ability to drive NRF2 degradation.

In preclinical models, these KEAP1 activators led to robust suppression of NRF2 signaling and showed meaningful antitumor activity across several tumor types with NRF2 pathway activation. Importantly, pharmacologic NRF2 degradation also enhanced the effects of multiple chemotherapies and radiotherapy, supporting the therapeutic potential of KEAP1 activation in overcoming treatment resistance in NRF2-driven cancers. Collectively, these findings provide a strong mechanistic and translational rationale for the clinical evaluation of KEAP1 activators.

"By showing that KEAP1 can be pharmacologically activated, Vividion has pioneered a new therapeutic approach to treating NRF2-driven cancers," said Matt Patricelli, Ph.D., Chief Scientific Officer of Vividion. "Mechanistic insights from these studies informed the design of our clinical KEAP1 activator, VVD-037, and its rational combinations with other cancer therapies. We’re excited to continue to explore its potential across the many cancer types driven by NRF2 dysregulation."

VVD-037, Vividion’s lead KEAP1 activator, is currently being evaluated in a Phase I clinical trial (NCT05954312) in patients with solid tumors characterized by NRF2 pathway activation.

(Press release, Vividion Therapeutics, DEC 22, 2025, View Source [SID1234661583])

On December 22, 2025 Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) reported it will webcast its presentation at the 44th Annual J.P. Morgan Healthcare Conference on Monday, January 12, 2026. The presentation is scheduled for 2:15 p.m. Pacific Time (5:15 p.m. Eastern Time) and may be accessed from the "Investors & Media" page of Regeneron’s website at View Source A replay and transcript of the webcast will be archived on the Company’s website for at least 30 days.

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(Press release, Regeneron, DEC 22, 2025, View Source [SID1234661582])

On December 22, 2025 Propanc Biopharma, Inc. (Nasdaq: PPCB) ("Propanc" or the "Company"), a biopharmaceutical company developing novel treatments for chronic diseases such as recurrent and metastatic cancer, reported that the Company and its joint research partners at the Universities of Jaén and Granada published key findings in a peer reviewed journal, Scientific Reports, regarding the impact of proenzymes on pancreatic ductal adenocarcinoma (PDAC) fibroblasts. From the publishers of Nature, Scientific Reports is an online, open access journal, which publishes primary research from all areas of the natural and clinical sciences. The article is entitled, "Impact of pancreatic proenzymes on pancreatic ductal adenocarcinoma associated fibroblasts," and available online. The tumor microenvironment (TME) plays a pivotal role in tumor initiation, progression, and the form of pre-metastatic niches. PDAC is characterized by a dense fibrotic stroma containing a significant enriched population of cancer-associated fibroblasts (CAFs). The interplay between CAFs and tumor cells is crucial in driving tumor advancement and metastasis, underscoring the potential benefits of novel therapeutic strategies targeting stromal cells to improve patient survival. PRP, consisting of two bovine derived pancreatic proenzymes, trypsinogen and chymotrypsinogen, have shown efficacy in cancer treatment. The findings demonstrate PRP exerts multifaceted effects. Results underscore the candidacy of PRP as a potential disruptor of the TME.

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Future clinical investigation is planned to validate the translational potential of PRP as an adjunct therapy for PDAC patients who no longer respond to standard treatment regimen. Despite recent advancements in clinical management, PDAC remains one of the most aggressive and deadliest forms of cancer, projected to become the second leading cause of cancer-related deaths by 2030. PDAC is characterized by its late-stage diagnosis, limited treatment options, and poor prognosis.

"Our findings demonstrate that PRP exerts multifaceted effects specifically over the CAFs population and tumor cells. All together, these results highlight PRP as a promising adjunct therapeutic candidate capable of disrupting key interactions within the PDAC TME," said Dr. Belén Toledo, PhD, joint lead researcher from the University of Jaén.

"After several years of research pioneered with our scientific researchers, we find ourselves publishing compelling scientific evidence that PRP has the potential to dramatically alter the way we perceive poor patients diagnosed with this killer disease," said Mr. James Nathanielsz, Propanc’s Chief Executive Officer. "We plan to undertake our Phase 1b study in advanced cancer patients suffering from solid tumors in Q3, 2026, and further announcements are anticipated. This pivotal study will determine our target dose for Phase 2 studies in which PDAC is one of our target therapeutic indications. We look forward to advancing PRP into the clinic as soon as possible to help PDAC patients with such a poor survival prognosis."

(Press release, Propanc, DEC 22, 2025, View Source [SID1234661581])

On December 22, 2025 Promontory Therapeutics Inc., a clinical stage pharmaceutical company advancing small molecule oncology approaches with immunotherapeutic effects, reported that the pre-specified efficacy requirement of its Phase 2 study of PT-112 for recurrent thymoma has been exceeded.

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Patients with recurrent thymoma have limited options for standard of care treatment, and there is no drug approved for this indication in the US, the European Union or Japan.

Of the first ten patients with thymoma assessed for tumor response in an ongoing phase 2 clinical trial at the NCI, three (30%) had experienced RECIST partial responses, an objective response rate that numerically exceeds that of the recent Phase 2 monotherapy data in the public domain with current off-label treatment options. PT-112 is well tolerated, and no new safety signals were observed. Patients treated with a dosing regimen based upon the PT-112 recommended Phase 3 dose (RP3D) achieved durable disease control without symptomatic toxicities, and no discontinuations due to adverse events (AEs). The PT-112 RP3D was agreed with the FDA at a recent end of Phase 2 (EOP2) Meeting on the separate PT-112 program in metastatic castration-resistant prostate cancer (mCRPC).

After reaching the interim efficacy requirement, enrollment of patients with recurrent thymoma continues at the National Cancer Institute (NCI), the single site leading the Phase 2 study of PT-112 under a formal Collaborative Research and Development Agreement (CRADA) with Promontory Therapeutics (NCT05104736).

At the American Association of Cancer Research (AACR) (Free AACR Whitepaper) 2025 Annual Meeting, the investigators from the NCI presented data on anti-cancer immune responses among the first 15 thymic epithelial tumor (TET) patients treated with PT-112 monotherapy, with increases in both adaptive (CD8+ and CD4+) and innate (NK) cell types reaching statistical significance. This led to the investigators’ conclusion that "PT-112 induces robust signals of immune activation… across the adaptive and innate immune systems… indicative that PT-112’s immune effects play a significant role in its anti-cancer mechanism1"

Consistent with the AACR (Free AACR Whitepaper) data, recent on-treatment biopsies show increased CD8+ T cell infiltration in tumor tissue and absence of viable tumor in two participants with stable disease to date per RECIST.

Patients with thymoma are at risk for paraneoplastic autoimmune diseases, which in turn increases the risk of immune-related AEs (irAEs) that can occur with T cell-directed immunotherapy. irAEs with PT-112 are uncommon, and the risk is not higher than that observed with conventional systemic therapies. Early observations of an absence of increased incidence of new-onset irAEs in patients with thymoma receiving PT-112, coupled with evidence of clinical and immune activity, provides a unique opportunity to offer a novel immunomodulatory treatment that does not increase the risk of immune toxicity.

Promontory Therapeutics is planning the next stage of development of PT-112 in recurrent thymoma, and the company leadership will be participating in industry partnering meetings during the JPMorgan Healthcare conference week (week of January 12th) in San Francisco.

(Press release, Promontory Therapeutics, DEC 22, 2025, View Source [SID1234661580])