PI3K inhib 
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  • ||||||||||  Journal:  Tanshinone IIA alleviates IL-1?-induced chondrocyte apoptosis and inflammation by regulating FBXO11 expression. (Pubmed Central) -  Apr 28, 2024   
    Curcumin alone led to dose-dependent responses and when combined with BYL719, positive effects were revealed, as they were when it was combined with MK-1775 or PD-0332991, suggesting a potential use of some of these combinations for HPV+ OPSCC. TAN IIA inhibits PI3K/Akt and NF-?B pathways by down-regulating FBXO11 expression, alleviates chondrocyte apoptosis and inflammation, and delays the progression of OA.
  • ||||||||||  Review, Journal:  The Role of Curcumin in Cancer: A Focus on the PI3K/Akt Pathway. (Pubmed Central) -  Apr 27, 2024   
    Curcumin has been found to inhibit the PI3K/Akt pathway in tumor cells, primarily via the regulation of different key mediators, including growth factors, protein kinases, and cytokines. This review presents the therapeutic potential of curcumin in different malignancies, such as glioblastoma, prostate and breast cancer, and head and neck cancers, through the targeting of the PI3K/Akt signaling pathway.
  • ||||||||||  Journal:  Marine-Fungus-Derived Natural Compound 4-Hydroxyphenylacetic Acid Induces Autophagy to Exert Antithrombotic Effects in Zebrafish. (Pubmed Central) -  Apr 26, 2024   
    Using a zebrafish model, we found that HPA had a strong antithrombotic activity because it can significantly increase cardiac erythrocytes, blood flow velocity, and heart rate, reduce caudal thrombus, and reverse the inflammatory response caused by Arachidonic Acid (AA). Further transcriptome analysis and qRT-PCR validation demonstrated that HPA may regulate autophagy by inhibiting the PI3K/AKT/mTOR signaling pathway to exert antithrombotic effects.
  • ||||||||||  LY294002 / Eli Lilly
    Journal, IO biomarker:  Endogenous ?3-adrenergic receptor activation alleviates sepsis-induced cardiomyocyte apoptosis via PI3K/Akt signaling pathway. (Pubmed Central) -  Apr 25, 2024   
    Inhibition of PI3K using LY294002 abolished the inhibitory effect of BRL37344 on LPS-induced caspase-3, -8, and -9 activation in H9c2 cells...SR59230A not only increased myocardial apoptosis, reduced p-AktSer473 and Bcl-2 contents, but also increased mitochondrial Bax, cytoplasm cytochrome c, cleaved caspase-9 and cleaved caspase-3 levels of the myocardium in septic rats. These results suggest that endogenous ?3-AR activation alleviates sepsis-induced cardiomyocyte apoptosis via PI3K/Akt signaling pathway and maintains intrinsic myocardial systolic function in sepsis.
  • ||||||||||  Preclinical, Review, Journal:  Strategies and techniques for preclinical therapeutic targeting of PI3Kin oncology: where do we stand in 2024? (Pubmed Central) -  Apr 22, 2024   
    We discuss the current landscape of PI3K inhibitors in preclinical and clinical trials, address the mechanisms of resistance to PI3K inhibition along with their associated toxic effects, and highlight significant advancements in preclinical research of this field. Based on our study and comprehension of PI3K, we provide a recapitulation of the key lessons learned from the research process and propose potential measures for improvement that could prove valuable.
  • ||||||||||  tamoxifen / Generic mfg.
    Journal, Epigenetic controller:  Underlying anti-cancer mechanisms of histone deacetylase (HDAC) inhibitors in tamoxifen-resistant breast cancer cells. (Pubmed Central) -  Apr 22, 2024   
    This study aimed to explore the underlying mechanisms of histone deacetylase (HDAC) inhibitor trichostatin A (TSA) to overcome resistance to tamoxifen in breast cancer cells...Finally, expression of vascular endothelial growth factor (VEGF), E-cadherin, Vimentin, phosphorylated phosphatidylinositol kinase (p-PI3k), phosphorylated protein kinase B (p-AKT), and phosphorylated mammalian target protein of rapamycin (p-mTOR) was evaluated by western blotting...However, HDAC inhibitor combined with PI3K inhibitor exerts more profound effects on the cancer cells as compared to HDAC inhibitor monotherapy. HDAC inhibitors inhibited the survival of breast cancer drug-resistant cells, invasion, migration, and angiogenesis by inhibiting the PI3k/Akt/mTOR signaling pathway.
  • ||||||||||  Aliqopa (copanlisib) / Bayer
    Journal, Benefit-risk assessment:  Model-Based Benefit/Risk Analysis for the Copanlisib Intermittent Dosing Regimen. (Pubmed Central) -  Apr 18, 2024   
    Exposure-safety analyses revealed a borderline significant linear relationship for grade??3 TEAEs and no significant exposure-safety relationships for other investigated safety end points. The model-based benefit/risk framework considered the established exposure-response models and defined clinical utility function which confirmed the appropriateness of the copanlisib dosing regimen across the range of its achieved exposures.
  • ||||||||||  bleomycin / Generic mfg.
    Journal:  Qingkailing granule alleviates pulmonary fibrosis by inhibiting PI3K/AKT and SRC/STAT3 signaling pathways. (Pubmed Central) -  Apr 15, 2024   
    In vivo, QKL reduced collagen deposition and suppressed proinflammatory cytokines in a bleomycin-induced PF mouse model...Molecular docking simulations highlighted interactions between QKL's active compounds and key proteins, showing inhibitory effects on epithelial damage and fibrosis. Collectively, these findings underscore the therapeutic potential of QKL in alleviating pulmonary inflammation and fibrosis through the downregulation of PI3K/AKT and SRC/STAT3 signaling pathways, with a pivotal role attributed to its active compounds.
  • ||||||||||  pramipexole IR / Generic mfg., sirolimus / Generic mfg.
    Preclinical, Journal:  ?-Asarone inhibitsAutophagy by activating the PI3K/Akt/mTOR Pathway in a Rat Model of Depression in Parkinson's Disease. (Pubmed Central) -  Apr 15, 2024   
    Collectively, these findings underscore the therapeutic potential of QKL in alleviating pulmonary inflammation and fibrosis through the downregulation of PI3K/AKT and SRC/STAT3 signaling pathways, with a pivotal role attributed to its active compounds. We concluded that ?-asarone might improve the behavior of DPD model rats by activating the PI3K/Akt/mTOR pathway, inhibiting autophagy and protecting neuron.
  • ||||||||||  irinotecan / Generic mfg.
    Journal:  Ginsenoside Rh4 alleviates gastrointestinal mucositis and enhances chemotherapy efficacy through modulating gut microbiota. (Pubmed Central) -  Apr 13, 2024   
    In summary, our findings confirm that ginsenoside Rh4 can alleviate CPT-11-induced gastrointestinal mucositis and enhance the anti-tumor activity of CPT-11 by modulating gut microbiota and its related metabolites. Our study validates the potential of ginsenoside Rh4 as a modulator of the gut microbiota and an adjunctive agent for chemotherapy, offering new therapeutic strategies for addressing chemotherapy side effects and improving chemotherapy efficacy.
  • ||||||||||  Inlyta (axitinib) / Pfizer
    Preclinical, Journal:  Knockdown of the VEGFB/VEGFR1 signaling suppresses pubertal mammary gland development of mice via the inhibition of PI3K/Akt pathway. (Pubmed Central) -  Apr 10, 2024   
    In this study, we observed that blocking the VEGF receptors with Axitinib suppressed the pubertal mammary gland development...Finally, the knockdown of VEGFB and VEGFR1 suppressed the pubertal development of mice mammary gland with the inhibition of the PI3K/Akt pathway. In summary, the results showed that knockdown of the VEGFB/VEGFR1 signaling suppresses pubertal mammary gland development of mice via the inhibition of the PI3K/Akt pathway, which provides a new target for the regulation of pubertal mammary gland development.
  • ||||||||||  Journal:  Dose optimization for cancer treatments with considerations for late-onset toxicities. (Pubmed Central) -  Apr 9, 2024   
    We illustrate a re-design of this trial to compare the approach to those that only consider early toxicity outcomes and disregard late-onset toxicities. We also provide proposals going forward for dose optimization in early development of novel anticancer agents with considerations for late-onset toxicities.