LAST WEEK TODAY!

A summary of what was published on ProstateWarriors.com during the past week

Here I am with the sixth newsletter from the site. This week it will be more about preclinical than clinical research, but there are still good news!

We also have a podcast if you prefer to listen to the newsletter, you can find it HERE.​

Clinical Research

• Xaluritamig (AMG 509) Phase 3 Trial: A Phase 3 clinical trial is scheduled to begin enrolling patients in January 2025 to evaluate xaluritamig for metastatic castration-resistant prostate cancer (mCRPC). This study will compare xaluritamig to standard treatments such as cabazitaxel or a second androgen receptor-directed therapy (ARDT). The trial will include patients with mCRPC who have previously been treated with at least one ARDT and one taxane therapy.
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• VVD-130850 Phase I Trial: A Phase I clinical trial is underway to assess the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary anti-tumor activity of VVD-130850, a small-molecule inhibitor targeting the STAT3 transcription factor in advanced solid and hematologic tumors, including prostate cancer. This oral drug will be tested as a standalone therapy and in combination with checkpoint inhibitors.
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• Copper-61 Radiotracer Phase I Trial: A Phase I clinical trial is underway to evaluate the safety and effectiveness of a novel molecular imaging (MI) radiotracer using Copper-61 (61Cu) to image prostate cancer. The study will use 61Cu-NODAGA-PSMA, which targets Prostate Specific Membrane Antigen (PSMA). The primary goal is to assess the safety of the radiotracer, and secondary objectives include dosimetry calculations and determining the effectiveness of 61Cu-NODAGA-PSMA by calculating the number of suspected PSMA-positive malignant lesions observed.
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• AR-ctDETECT Blood Test:ÂA new blood test called AR-ctDETECT can differentiate between patients with advanced prostate cancer who have poor and favorable prognoses. This test analyzes circulating tumor DNA (ctDNA) in the blood. The detection of ctDNA is linked to worse overall survival and is specific to genes relevant to prostate cancer and hormone resistance.
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Preclinical Research

• CRISPR Gene Editing:ÂResearchers have utilized the CRISPR-Cas13Âgene editing tool to selectively silence cancer-causing gene mutations by targeting RNA. This method allows for the degradation of mutant RNA while sparing healthy RNA, potentially leading to personalized treatments with reduced side effects. This approach has demonstrated precision and adaptability and overcomes limitations of earlier CRISPR applications.
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• Bone-Modifying Agents and Survival: A study found that bone-modifying agents, such as bisphosphonates (zoledronic acid) and denosumab, are associated with improved overall survival in patients with metastatic castration-resistant prostate cancer (mCRPC)7. The study noted a significant improvement in overall survival for the group that received bone-modifying agents (58 months vs. 45 months)8. However, there were no significant differences in progression-free survival between the groups.
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• Dinuclear Platinum(II) Complexes: A study investigated the potential of azolato-bridged dinuclear platinum(II) complexes, particularly 5-H-Y, as a possible alternative to cisplatin for treating prostate cancer. These complexes have shown strong cytotoxic effects and the ability to inhibit AR signaling, with lower acute toxicity compared to traditional platinum-based drugs.
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• Metformin Mechanism:ÂResearch has provided direct evidence that the diabetes drug metformin lowers blood sugar by interfering with mitochondria, specifically by blocking mitochondrial complex I. This action reduces the cell’s energy supply and may contribute to the drug’s diverse health benefits, including potential anti-cancer effects.
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• Targeting Mitochondrial HSP60:ÂResearch has identified HSP60 as a potential treatment target for neuroendocrine prostate cancer (NEPC). Inhibiting HSP60 was found to reduce β-catenin signaling and caused neuroendocrine cells to revert to a cisplatin-sensitive state, which could increase the effectiveness of existing drugs.
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• Starving Prostate Cancer Tumors: Researchers have discovered that prostate cancers can be effectively destroyed by inhibiting both GCN2 and p53 proteins. This method exploits metabolic vulnerabilities unique to prostate cancer, as these proteins are involved in tumor cell survival and nutrient gathering.
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• Genomic Knowledgebase: Genomenon has developed the G3 knowledgebase, a comprehensive, searchable database of clinically relevant genomic information. The G3 knowledgebase uses an AI platform and a genomic-specific large language model (LLM) to accelerate discoveries and advancements in patient care and includes a wide array of information including genes, variants, gene-disease relationships, drugs, and patient demographics.

And…that’s all folks! For today at least!
Please let me know if there is anything I can improve in my newsletters, and let me know if you have enjoyed the podcast.

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Have a great weekend!

Max