On April 7, 2024 Ascentage Pharma (6855.HK), a global biopharmaceutical company engaged in developing novel therapies for cancer, age-related diseases, and chronic hepatitis B (CHB), reported that it releases the latest results from three preclinical studies of its novel drug candidates olverembatinib, MDM2-p53 inhibitor alrizomadlin (R&D Code: APG-115), FAK/ALK/ROS1 tyrosine kinase inhibitor APG-2449, and embryonic ectoderm development (EED) inhibitor APG-5918, at the 2024 American Association of Cancer Research Annual Meeting (AACR 2024) (Press release, Ascentage Pharma, APR 7, 2024, View Source;ascentage-pharma-presents-results-from-three-studies-at-2024-american-association-of-cancer-research-annual-meeting-302109949.html [SID1234641849]). This year’s AACR (Free AACR Whitepaper) annual meeting will be held from April 5-10 2024, in San Diego, California, USA.

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"We are pleased to present the preclinical research data of four assets in our pipeline at the AACR (Free AACR Whitepaper) 2024. The results provided essential support for the potential clinical development and therapeutic combinations of these compounds in SDH-deficient neoplasms, prostate cancer, and ovarian cancer," said Dr. Yifan Zhai, Chief Medical Officer of Ascentage Pharma. "Moving forward, we will continue to advance these programs toward the clinical stage in order to bring more treatment options to patients in need."

The details of these three preclinical studies are as follows:

Olverembatinib, a novel multikinase inhibitor, demonstrates superior antitumor activity in succinate dehydrogenase (SDH)-deficient neoplasms

Abstract#: 1971

Time: Monday April 8, 2024, 9:00 AM – 12:30 PM (Pacific Time)

Introduction:

Succinate dehydrogenase (SDH) – deficient (dSDH) neoplasms are identified by the loss of immunohistochemical expression of SDHB due to the bi-allelic inactivation of any of the four components of mitochondrial SDH complex (SDH A-D).
Succinate accumulation, due to SDH deficiency, is involved in tumorigenesis of different types of cancers including gastrointestinal stromal tumor (GIST), paraganglioma, pheochromocytoma, renal cell carcinoma, pituitary adenomas, and pancreatic neuroendocrine tumors.
The prognosis of patients with dSDH neoplasia, especially GIST, is poor and approved tyrosine kinase inhibitors (TKIs) have limited efficacy. There is a high unmet medical need for these patients.
Olverembatinib, a novel multi-kinase inhibitor, targets a broad spectrum of kinases and has demonstrated promising efficacy in dSDH GIST patients in an ongoing phase I clinical trial. In this study, we assessed antitumor effects of olverembatinib in preclinical models of dSDH cancers and dSDH GIST primary tumor cells, and explored potential mechanisms of action.
Conclusions:

Olverembatinib showed superior anti-tumor activity in dSDH cell lines in vitro and human dSDH GIST primary tumor cells ex vivo.
Olverembatinib, as a multi-target kinase inhibitor, exerted antitumor effects by modulating multiple signaling pathways including hypoxia, angiogenesis, apoptosis, proliferation, and survival, which are involved in tumorigenesis of dSDH cancers.
Olverembatinib demonstrated more potent in vivo antitumor activity in mice bearing PC12#5F7 (SDHB KD) xenograft tumors than other TKIs. Western blot analysis in tumor tissues collected from mice further confirmed the modulation of the signal pathways by olverembatinib observed in cell lines.
In summary, the results provide a rationale for future clinical development of olverembatinib in dSDH cancers.
Embryonic ectoderm development (EED) inhibitor APG-5918 (EEDi-5273) and MDM2 inhibitor alrizomadlin (APG-115) synergistically inhibit tumor growth in preclinical models of prostate cancer (PCa)

Abstract#: 3223

Time: Monday April 8, 2024, 1:30 PM – 5:00 PM (Pacific Time)

Introduction:

Prostate cancer (PCa) is one of the most frequently diagnosed malignancies among elderly males. Androgen deprivation therapy (ADT) with or without androgen receptor (AR) inhibitors is widely used as initial treatment for advanced PCa. However, most ADT-treated patients eventually develop castration-resistant prostate cancer (CRPC), which is in urgent need of novel therapies.
Polycomb repressive complexes 2 (PRC2) dysregulation is common in PCa and correlates with poor prognosis. PRC2 mediates histone H3 lysine 27 tri-methylation (H3K27me3), a repressive epigenetic marker for gene transcription. embryonic ectoderm development (EED), a PRC2 core component, is crucial for histone methyltransferase activity through direct binding to H3K27me3.
MDM2, a negative regulator of the tumor suppressor p53, is frequently amplified or overexpressed in PCa, and associated with poor clinical outcomes and metastasis.
The aim of this study was to evaluate antitumor activity and molecular mechanisms of the investigational, clinical-stage EED inhibitor APG-5918/EEDi-5273 and MDM2 selective inhibitor alrizomadlin (APG-115) in PCa preclinical models
Conclusions:

In PCa preclinical models, the combination of APG-5918 and alrizomadlin synergistically inhibited cellular proliferation and induced cellular apoptosis.
APG-5918 in combination with alrizomadlin synergistically enhanced antitumor activity in PCa xenograft models in vivo.
Mechanistically, PD analysis revealed that APG-5918 downregulated the oncogenic DNA methylation factors (UHRF1, DNMT1) and histone methylation marker H3K27me3. Alrizomadlin markedly downregulated UHRF1 and DNMT1, and upregulated p53 and p21 expression. Combined treatment further enhanced downregulation of DNMT1, UHRF1, cell cycle pathway proteins (pRb, CDK6), antiapoptotic protein MCL-1, and synergistically increased cleavage of PARP-1, a marker of apoptosis.
Therefore, the findings provide a scientific rationale for future clinical development of APG-5918 and alrizomadlin to treat patients with PCa.
APG-2449, a novel focal adhesion kinase (FAK) inhibitor, inhibits metastasis and enhances the antitumor efficacy of PEGylated liposome doxorubicin (PLD) in epithelial ovarian cancer (EOC)

Abstract#: 4569

Time: Tuesday April 9, 2024, 9:00 AM – 12:30 PM (Pacific Time)

Introduction:

Ovarian cancer is among the leading causes of cancer-related death in women, and most cases are diagnosed at later stages with distant metastasis.
FAK overexpression or activation occurs in a substantial proportion of epithelial ovarian cancers (EOCs) and is predictive of poor clinical outcomes.
FAK plays an important role in cell migration and chemoresistance, rendering FAK inhibition a promising treatment approach to reduce metastasis of tumor cells and sensitize them to chemotherapy. FAK is therefore emerging as a potential treatment target.
The aim of this study was to evaluate the antitumor efficacy of investigational APG-2449, a novel FAK inhibitor, combined with PLD, a commonly used chemotherapy, in relapsed or refractory ovarian cancer.
Conclusions:

APG-2449 combined with doxorubicin showed synergistic antiproliferative effects in both platinum-resistant and platinum-sensitive ovarian cancer cell lines.
FAK inhibition via APG-2449 alone attenuated migration of ovarian cancer cells in a dose-dependent manner.
APG-2449 in combination with PLD showed enhanced antitumor activity in platinum-resistant OVCAR-3 ovarian cancer CDX model.
The combination regimen prolonged ascites-free and survival times in the ID8-Luc peritoneal syngeneic model.
These promising results support the future clinical development of this combination treatment for ovarian cancer.

On April 7, 2024 Affini-T Therapeutics, Inc., a precision immunotherapy company unlocking the power of T cells against oncogenic driver mutations, reported that management is presenting data from the company’s oncogenic driver programs targeting HLA-A*11:01 KRAS G12D and HLA-A*02:01 p53 R175H at this year’s American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2024 in San Diego (Press release, Affini-T Therapeutics, APR 7, 2024, View Source [SID1234641850]). In addition, the team is presenting two trial-in-progress posters for Affini-T’s Phase 1 clinical-stage programs targeting KRAS G12V, the company-sponsored AFNT-211 study and the Fred Hutchinson Cancer Center investigator-initiated AFNT-111 study at AACR (Free AACR Whitepaper).

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"We are excited to be at AACR (Free AACR Whitepaper) unveiling new preclinical data, which includes a closer look at the promise of our novel non-viral TRAC-knocked-in T cell therapy for the treatment of p53 R175H-mutant solid tumors," said Loïc Vincent, Ph.D., Chief Scientific Officer, Affini-T Therapeutics. "We are also proud to present preclinical data from our cell therapy targeting KRAS G12D, which highlights the promising potential of our proprietary non-viral knock-in THRIVE platform. These findings continue to motivate our team as we advance programs leveraging TCR-engineered T cells as potential paradigm-shifting treatments for patients with solid tumor cancers."

Poster presentation details are as follows:

AFNT-212: A TRAC-knocked-in KRAS G12D-specific TCR-T cell product enhanced with CD8αβ and a chimeric cytokine receptor for treatment of solid cancers

Abstract #5973, Session: Adoptive Cell Therapies 1: Tumor Antigen-Specific T-cells and TCR-T
Session Date/Time: Sunday, April 7, 2024, 1:30 PM – 5:00 PM
Presenting Author: Loïc Vincent, Ph.D., Chief Scientific Officer, Affini-T Therapeutics
Summary: AFNT-212-engineered TCR-T cells showed high functional avidity and in vitro cytotoxicity against KRAS G12D-positive tumor cell lines, including CL40 (colon), PANC-1 and HPAF-II (pancreas), SK-LU-1 (lung), HuCCT1 (cholangiocarcinoma), etc. Additionally, engineered TCR-T cells demonstrated robust and durable anti-tumor activity in vivo and low risk of off-target/off-tumor toxicity. Affini-T’s proprietary non-viral knock-in (KI) THRIVE platform achieved high transgene integration efficiency and cell growth to yield relevant numbers of engineered TCR-T cells for clinical application. The study supports the planned clinical investigation of the novel KRAS G12D mutant TCR-engineered CD4+ and CD8+ T cell therapy in 2024.
Non-viral engineered T cell therapy specific for the hotspot mutation p53 R175H that integrates signal 1 (TCR), signal 2 (co-stimulation) and signal 3 (cytokine) and co-opts FasL-dependent apoptosis to achieve a coordinated antitumor CD4/8 T cell response

Abstract #7242, Session: Adoptive Cell Therapies 1: Tumor Antigen-Specific T-cells and TCR-T
Session Date/Time: Sunday, April 7, 2024, 1:30 PM – 5:00 PM
Presenting Author: Gary Shapiro, Ph.D., VP Biology Discovery, Affini-T Therapeutics
Summary: The tumor suppressor TP53 is the most frequently mutated gene across human cancers, with a highly recurrent arginine to histidine hotspot alteration in codon 175 leading to novel tumor-dependent functions. In this study, we reported the use of a novel CRISPR-Cas nuclease system to knock in a six-gene multi-cistronic cassette into the TRAC locus with high efficiency. We employed several strategies to maximize the potency and durability of a TCR-T cell product targeting the p53 R175H oncogenic driver, TCR, co-stimulation and cytokine signaling – which delivered full stimulation of both CD8+ and CD4+ T cells. These data support the planned clinical development of a novel non-viral TRAC-knocked-in T cell therapy for the treatment of p53 R175H-mutant solid tumors.

On April 7, 2024 Edgewood Oncology, a clinical-stage biotechnology company focused on delivering BTX-A51 to patients with hematologic malignancies and genetically-defined solid tumors, reported the publication of new preclinical data from a study of BTX-A51 in human liposarcoma (LPS) conducted by Dana-Farber Cancer Institute and Hebrew University-Hadassah Medical School to be presented at the AACR (Free AACR Whitepaper) Annual Meeting 2024 in San Diego (Press release, Edgewood Oncology, APR 7, 2024, View Source [SID1234641851]). BTX-A51 is a first-in-class, small molecule, multi-selective kinase inhibitor of casein kinase 1 alpha (CK1α) as well as the transcriptional regulators cyclin-dependent kinases 7 and 9 (CDK7 and CDK9) that synergistically co-targets master regulators of cancer to promote programmed cell death, or apoptosis.

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The presentation (Abstract 604), "Targeting casein kinase 1 alpha (CK1alpha) and transcriptional CDKs (CDK7/9) in human liposarcomas," highlighted findings for BTX-A51 in preclinical human models of LPS. The data demonstrate that BTX-A51 has preclinical efficacy in treating patient-derived LPS in cell lines and human xenograft models and provides insight into the synergy gained by inhibiting both CK1α and CDK9.

"Dedifferentiated liposarcomas (DDLPS) are rare tumors derived from precursors of fat cells which can occur anywhere in the body. Patients with metastatic DDLPS face a life-threatening disease in need of more effective therapeutic options, which we hope to develop by taking advantage of vulnerabilities in LPS that have been uncovered by recent research on the abnormal DNA and other molecular characteristics of LPS," said George Demetri, M.D., Professor of Medicine and director of the Sarcoma Center at Dana-Farber. "Based on these data, we believe that it is justified to move BTX-A51 into a clinical trial for patients with LPS, which we will plan to open soon for enrollment."

Liposarcomas are universally characterized by amplification of the mouse double minute 2 homolog (MDM2) gene, which leads to destruction of the normal (non-mutated, also known as "wild type") p53. The data demonstrate that BTX-A51 significantly reduces the abnormal overexpression of MDM2 in multiple patient-derived LPS cell lines, leading to upregulation of p53 expression and ultimately apoptosis. Finally, BTX-A51 was demonstrated to be well-tolerated and effective in an LPS patient-derived xenograft model.

"We’re pleased that investigators at Dana-Farber have taken an interest in BTX-A51, which is currently being evaluated in a Phase 2 combination study with azacitidine in patients with relapsed or refractory (R/R) AML," said David N. Cook, Ph.D., chief executive officer of Edgewood Oncology. "These data also suggest the potential for BTX-A51 in cancers with MDM2 amplifications, a group of genetically defined tumors that span multiple tissue types suggesting broader potential."

Additional Details about the Study

Using three different CDK9-selective inhibitors in human LPS cell lines, the authors showed that CDK9 inhibition suppressed cell growth and induced apoptosis by decreasing MDM2 levels while inducing expression of p53. It was also demonstrated that the potency of CDK9 inhibitors is significantly enhanced upon CK1α depletion. These data led to the investigation of BTX-A51, which targets CK1α and CDK9 as well as CDK7, in LPS cells and has previously been shown to inhibit these kinases with nanomolar efficacy in AML models. BTX-A51 potently reduced expression of MDM2 with marked induction of p53, resulting in apoptosis of LPS cells. BTX-A51 also reduces expression of MCL1 and primes LPS cell lines and primary LPS cells for BIM-induced apoptosis, as demonstrated by BH3 profiling. Importantly, preliminary in vivo data in an LPS patient-derived xenograft model reveal that BTX-A51 is well-tolerated under conditions that inhibit tumor growth.

On April 7, 2024 BioNTech SE (Nasdaq: BNTX, "BioNTech" or "the Company") reported three-year follow-up data from a Phase 1 trial with the mRNA-based individualized neoantigen-specific immunotherapy ("iNeST") candidate autogene cevumeran (also known as BNT122, RO7198457) in patients with resected pancreatic ductal adenocarcinoma ("PDAC") (Press release, BioNTech, APR 7, 2024, View Source [SID1234641837]). The data show that in 8 out of 16 patients autogene cevumeran elicited an immune response up to three years post administration measured by activated T cells. The persistence of T cels was associated with a longer median recurrence-free survival in cancer vaccine responders.

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"These new data are an early signal for the potential of our individualized mRNA cancer vaccine approach in this indication with an unmet medical need. The results indicate that our uridine mRNA-LPX technology can promote activation of cytotoxic T cells that may help to eliminate residual tumor foci at early stages of the disease to delay or prevent recurrence," said Prof. Özlem Türeci, M.D., Co-Founder and Chief Medical Officer at BioNTech. "Our ongoing Phase 2 trial with Genentech aims to confirm these findings on benefit for patients with PDAC compared with the current standard of care treatment in the post-surgical, adjuvant setting in a larger patient population. We remain committed to our vision of personalized cancer medicine and aim to help advance the standard of care for many patients."

The results featured in an oral presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) ("AACR") Annual Meeting 2024 show the following:

In 8 of 16 patients, autogene cevumeran elicited high-magnitude T cells specific to the encoded neoantigens.
98% of the T cells targeting individual neoantigens on the tumor and induced by autogene cevumeran were de novo in that they were not detected in blood, tumors, and adjacent tissues prior to administration of the investigational treatment.
Over 80% of the vaccine-induced neoantigen-specific T cells could still be detected up to three years post administration in patients with an immune response. These patients showed a prolonged median recurrence-free survival compared to non-responders.
6 of 8 patients with an immune response to autogene cevumeran remained disease free during the three-year follow-up period, while 7 of the 8 patients without an immune response to the treatment during the trial showed tumor recurrence.
The investigator-initiated, single center Phase 1 trial (NCT04161755) evaluated the safety of autogene cevumeran in sequential combination with the anti-PD-L1 immune checkpoint inhibitor atezolizumab and standard-of-care chemotherapy in 16 patients with resected PDAC. Data from the 1.5-year median follow-up were published in Nature in May 2023. The current data update includes a three-year median follow-up and was presented in a late-breaking oral presentation at the AACR (Free AACR Whitepaper) Annual Meeting 2024 in San Diego, California, by principal investigator Vinod Balachandran, M.D., surgeon-scientist at Memorial Sloan Kettering Cancer Center and principal investigator of the study.

An ongoing open-label, multicenter, randomized Phase 2 trial (NCT05968326), sponsored by Genentech in collaboration with BioNTech, was started in October 2023. The trial will investigate the efficacy and safety of adjuvant autogene cevumeran in combination with the anti-PD-L1 immune checkpoint inhibitor atezolizumab and chemotherapy compared with the current standard of care chemotherapy (mFOLFIRINOX) in patients with PDAC. The Phase 2 trial is currently enrolling patients at clinical trial sites in the United States, with additional sites planned to open globally. Autogene cevumeran is being jointly developed by BioNTech and Genentech and is currently being evaluated in three ongoing randomized Phase 2 clinical trials in adjuvant PDAC (as mentioned above), first-line melanoma, and adjuvant colorectal cancer.

About resected pancreatic ductal adenocarcinoma (PDAC)
PDAC is amongst the leading causes of cancer-related deaths in the United States4 with approximately 90% of patients dying within two years of their diagnosis5. A combination of surgical removal and systemic cytotoxic chemotherapy has shown to improve clinical outcomes; however, even with surgical resection, the relapse rate remains high, and the 5-year overall survival is only approximately 20%6 in patients who undergo surgery followed by adjuvant chemotherapy ("ACT") and only 8-10%i,ii in those who do not receive ACT. Thus, there is an unmet medical need for novel therapies for patients with resected PDAC.

About iNeST (individualized Neoantigen Specificimmuno Therapy)
iNeST immunotherapies are investigational individualized cancer therapies tailored to a specific patient’s tumor. They contain unmodified, pharmacologically optimized mRNA encoding up to 20 patient-specific neoantigens, identified using real-time next-generation sequencing and bioinformatic neoantigen discovery. Neoantigens are proteins that are produced by cancer cells that differ from the proteins produced by healthy cells and are recognized by immune cells. The mRNA is encapsulated in BioNTech’s proprietary intravenous RNA-lipoplex delivery formulation which is designed to enhance stability as well as enable targeted delivery to dendritic cells. By analyzing each patient’s tumor, BioNTech is able to identify the cancer mutations that may act as neoantigens. Each individual cancer vaccine encodes for neoantigen candidates with the highest likelihood of helping the immune system recognize the cancer. For this purpose, BioNTech has developed an on-demand manufacturing process, following Good Manufacturing Practice (GMP) conditions. Autogene cevumeran is currently being evaluated in various solid tumor indications, including three Phase 2 clinical trials in first-line melanoma, adjuvant colorectal cancer, and adjuvant pancreatic ductal adenocarcinoma.

An iNeST Fact Sheet and images from the iNeST manufacturing process are available in the newsroom section on BioNTech’s website at this link.

On April 7, 2024 HiFiBiO Therapeutics, a leading clinical stage global biotechnology company committed to advancing patient outcomes through single-cell precision, reported two posters at the AACR (Free AACR Whitepaper) 2024 meeting held on April 5-10, 2024, in San Diego, CA (Press release, HiFiBiO Therapeutics, APR 7, 2024, View Source [SID1234641870]).

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"One of the major challenges cancer immunotherapies face is the difficulties in selecting patients with tumors that will respond. Single-cell technologies can provide valuable insights into disease biology and help discern tumors that are more likely to respond; however, the lack of integrated data across diverse single-cell platforms hinders the potential of these novel technologies to inform clinical decisions." Jack Russella-Pollard, Ph.D., Executive Director, Translational Data Science, commented, "HiFiBiO has built an AI/ML powered curation and data integration process within our Drug Intelligence Science (DIS) translational platform that integrates publicly available datasets with in-house generated datasets to predict tumor response and guide target as well as indication selection."

Jinping Gan, Ph.D., Vice President, Global Head of Research, remarked: "Currently, there is no suitable model to describe complex tumor-immune interactions that can effectively guide clinical decisions. HiFiBiO has successfully constructed semi-mechanistic PKPD models for an anti-TNFR2 agonist and an anti-OX40 agonist that advocate for pulsatile agonism to achieve optimal anti-tumor efficacy. This innovative scientific work serves as a valuable tool for guiding dose and dose regimen optimization for the humanized versions of these T cell co-stimulatory agonists in clinical development."

By harnessing these cutting-edge technologies and tools within its DIS platform, HiFiBiO Therapeutics is steering the development of its drug candidates, including three antibodies currently undergoing Phase 1 evaluation: a first-in-class TNFR2 agonist (HFB200301, NCT05238883), a next-generation OX40 agonist (HFB301001, NCT05229601), and a best-in-class BTLA antagonist (HFB200603, NCT05789069).

These presentations underscore HiFiBiO Therapeutics’ unwavering commitment to innovation and its relentless pursuit of novel therapeutic solutions to address unmet medical needs.

Details on the poster presentations are as follows. E-Posters will be posted on HiFiBiO’s website following the live presentations.

Abstract Number: 6202

Title: Integrating public single-cell transcriptomics and patient profiles to guide clinical development

Presenter: Jack Russella-Pollard, Ph.D., Executive Director, Translational Data Science
Session Category: Bioinformatics / Computational Biology / Systems Biology / Convergent Science

Session Title: Integrative Cancer Science

Session Date and Time: Tuesday Apr 9, 2024, 1:30 PM – 5:00 PM

Location: Poster Section 36

Poster Board Number: 5

View full abstract here.

Abstract Number: 7176

Title: Optimization of T cell co-stimulatory agonists: A semi-mechanistic PKPD model integrating drug properties and tumor-immune interactions

Presenter: Jinping Gan, Ph.D., Vice President, Global Head of Research

Session Category: Experimental and Molecular Therapeutics

Session Title: Pharmacology and Pharmacogenetics

Session Date and Time: Wednesday Apr 10, 2024, 9:00 AM – 12:30 PM

Location: Poster Section 24

Poster Board Number: 17

View full abstract here.