Pointless putting much effort into presentations - with the way this company trashes capital management and I suspect operational mistakes.
So very brief recent NEW stuff - as the worth and potential of the actual drug skyrockets...
1/ $10 billion company Novocure - who have a form of targeted radiation produced a paper at this meeting - successfuly using Piquay (Alpelisib) A Pi3k drug not know to cross the blood brain barrier - with their radiation technology in GBM. Novocure talk positively about PI3k with radiation in other cancers.
Fields in Multiple Solid Tumor Types at the American Society for Radiation Oncology 2022 Annual Meeting
October 21, 2022
Highlights include an analysis of predictive biomarkers for overall survival and progression free survival in newly diagnosed glioblastoma patients
Pre-clinical research shows the potential for improved tumor control when Tumor Treating Fields are used with PULSAR in glioblastoma, PARP inhibitors in ovarian cancer and PI3K inhibitors in non-small cell lung cancer, GBM and ovarian cancer
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2/. (Astra Zeneca AKT drug verse PI3K / AKT / mTOR brain penetrant drug. )
26 October 2022 07:00 BST
Capivasertib, a potential first-in-class AKT inhibitor, combined with Faslodex could
become a new option for patients in this setting regardless of biomarker status
Positive high-level results from the CAPItello-291 Phase III trial showed that AstraZeneca’s capivasertib in combination with Faslodex (fulvestrant) demonstrated a statistically significant and clinically meaningful improvement in progression-free survival (PFS) versus placebo plus Faslodex in patients with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-low or negative locally advanced or metastatic breast cancer, following recurrence or progression on or after endocrine therapy (with or without a CDK4/6 inhibitor).
The trial met both primary endpoints, improving PFS in the overall patient population and in a prespecified biomarker subgroup of patients whose tumours had qualifying alterations in the PIK3CA, AKT1 or PTEN genes. Although the overall survival (OS) data were immature at the time of the analysis, early data are encouraging. The trial will continue to assess OS as a key secondary endpoint.
The safety profile of capivasertib plus Faslodex was similar to that observed in previous trials evaluating this combination.
Breast cancer is the most common cancer worldwide, with an estimated 2.3 million patients diagnosed in 2020.1 Approximately 70% of breast cancer tumours are considered HR-positive and HER2-low or negative.2 Endocrine therapies are widely used for the treatment of HR-positive breast cancer, but many patients with advanced disease develop resistance to 1st-line CDK4/6 inhibitors and estrogen receptor-targeting therapies, underscoring the need for additional options.3
Nicholas Turner, MD, PhD, Professor of Molecular Oncology at The Institute of Cancer Research, London, and The Royal Marsden NHS Foundation Trust, London, UK, and principal investigator in the CAPItello-291 Phase III trial, said: “The CAPItello-291 Phase III trial results show capivasertib offers a clinically meaningful improvement in progression free survival for patients with HR-positive breast cancer. This potential new medicine could give people more time with their cancer under control, which is a priority for patients and their families.”
Susan Galbraith, Executive Vice President, Oncology R&D, AstraZeneca, said: “These exciting data in an all-comers population indicate that capivasertib could become a new first-in-class treatment option for patients with HR-positive breast cancer. These patients often experience tumour progression on, or resistance to, available endocrine therapies for advanced disease and urgently need new therapies that extend the effectiveness of endocrine-based treatment approaches.”
The data will be presented at a forthcoming medical meeting and shared with global health authorities.
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3/ Finally comment of this actual chatline header announcement, in conjunction Huntsman Cancer Institute at the University of Utah in Salt Lake City, UT. (worth $300m into the value of paxalisib - my estimate)
Paxalisib superior,going head to head in this preclinic study - with other PI3k / AKT drugs
(HOW ABOUT FOR A CHANGE - SOMEBODY ELSE RESEARCH THE IMPORTANCE OF - FOR THE FIRST TIME MENTIONED, GENETIC SILENCING - THE COMPANY SURE WON'T EXPLAIN OR EVEN MENTION GENETIC SILENCING)
Conclusions and Future Directions
Genetic silencing of AKT induces melanoma cell death through suppression of downstream mTOR signaling and is dependent on functional kinase activity.
Genetic silencing is superior to pharmacological inhibition as it prevents reactivation of the PI3K>AKT pathway following relief of negative feedback.
Activated SGK1 can rescue lethal effects of siAKT123 knockdown.
Combination of AKT and SGK inhibition decreases melanoma cell proliferation and leads to increased overall survival in a BRAF-mutant melanoma mouse model but tumors still grow through treatment.
Second and third generation mTOR inhibition more effectively diminishes melanoma cell viability and leads to substantially increased overall survival.
Dual PI3K/mTOR inhibition may represent an effective therapeutic strategy in this refractory disease.
Next steps will be to test combination of PI3K/mTOR inhibitors with standard of care
Figure 3: A-D, Luminex quantitative immunoassay of phosphorylation of AKT (Ser473), P70S6 (Thr389), P-S6 (Ser235/236A, MTG001 cells treated with DMSO control, MK2206 (2.5µM), GDC0068 (1µM), INY-03-041 (500nM), GDC0941 (1µM), BYL719 (1µM), siAKT123 at 22 hours (50nM), or siAKT123 at 24 hours (50nM). E, Immunoblotting of cell lysates treated with DMSO control, MK2206 (2.5µM), GDC0068 (1µM), INY-03-041 (500nM), GSK0394 (3µM), GDC0941 (1µM), BYL719 (1µM), siAKT123 (50nM) at 22 hours, and siAKT123 (50nM) at 24 hours reveals complete knockdown of pAKT (Ser473) and total AKT by siAKT123 a
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