Notably, LY294002 (a PI3K inhibitor) and Anisomycin (a JNK activator) partially reversed the anti-apoptotic and anti-inflammatory effects of PTE, respectively. This study provides the first integrated evidence combining network pharmacology and experimental validation that PTE protects against LIRI by modulating the PI3K/AKT and JNK/c-Jun signaling pathways, offering novel pharmacological insights into its translational potential in LIRI.

P1, N=46, Recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jul 2027 | Trial primary completion date: Jun 2026 --> Jul 2027

P3, N=510, Recruiting, Jazz Pharmaceuticals | Trial completion date: Aug 2026 --> Jun 2028 | Trial primary completion date: Aug 2026 --> Jun 2028

P1, N=42, Recruiting, AstraZeneca | Not yet recruiting --> Recruiting | Trial completion date: Dec 2027 --> Jun 2026 | Trial primary completion date: Dec 2027 --> Jun 2026

The AKT inhibitor capivasertib has demonstrated clinical benefit in combination with the selective ER degrader fulvestrant in PIK3CA, PTEN and AKT-1 altered estrogen receptor positive breast cancer (ER+ BC). Rather than influencing gene expression, loss of KDM5C combined with capivasertib increased cell stress, DNA damage, cell cycle arrest and cell death. Collectively the data suggests that chromatin regulators may have different functions following capivasertib treatment, with inhibition having potential to enhance sensitivity to capivasertib in PIK3CA, PTEN and AKT-1 altered ER+ BC cells.

FGFR2 is lowly expressed in DFU and can exert a protective effect by activating the PI3K/Akt pathway. It is a candidate diagnostic biomarker and potential therapeutic target for DFU.

P2, N=57, Active, not recruiting, Royal Marsden NHS Foundation Trust | Recruiting --> Active, not recruiting | N=324 --> 57 | Trial completion date: Sep 2026 --> Jun 2027 | Trial primary completion date: Sep 2026 --> Jun 2027

P1/2, N=54, Recruiting, Celcuity Inc | Trial completion date: Nov 2027 --> Jan 2030 | Trial primary completion date: Nov 2025 --> Jan 2028

Furthermore, preliminary molecular docking analysis indicated potential binding affinity of A_443654 and A_770041 with the biomarker proteins, highlighting these compounds as candidates for further experimental investigation...A risk prediction model based on LOXL1, LOXL4, and SP6 was constructed and validated. The model, rather than individual genes, provides valuable insights, providing valuable insights for the diagnosis of GBM in the field of CSC and disulfidptosis.

Pharmacologic inhibition of AKT with the FDA-approved inhibitor capivasertib in Jak2V617F-transplanted mice similarly reduced splenomegaly and erythroid proliferation, mimicking the effects of Pitp β loss. Collectively, these results identify a novel PITPβ-PtdIns(3,4)P ₂ signaling axis that selectively maintains pathological AKT activation in JAK2V617F-driven MPN, revealing a promising therapeutic vulnerability.

Mechanistically, APOE overexpression significantly activated the PI3K/AKT signaling pathway, and this effect was effectively reversed by the PI3K inhibitor LY294002. Consistently, APOE overexpression enhanced tumor growth in vivo. These findings indicate that APOE promotes glioma progression through nuclear activity and activation of the PI3K/AKT signaling pathway, highlighting APOE-related signaling as a potential therapeutic target in glioma.

Prompt recognition, intensive management, and drug discontinuation are critical. This is one of the first case reports to describe sustained euglycemia following severe and refractory hyperglycemia due to capivasertib therapy.