pi3k in 22

PI3K-IN-22 is a dual kinase inhibitor of PI3Kα and mTOR, with IC50s of 0.9 and 0.6 nM respectively. PI3K-IN-22 could be used in cancer.

FAK-IN-22 (Compound 26) is an inhibitor of FAK, JAK3, and Aurora B, with IC50 values of 50.94 nM, 9.99 nM, and 0.49 nM, respectively, effectively suppressing tumorigenesis and metastasis in pancreatic ductal adenocarcinoma (PDAC). It inhibits proliferation in PANC-1 cells with an IC50 of 0.15 μM. FAK-IN-22 induces apoptosis and G2 M phase arrest in PANC-1 cells by inhibiting the FAK PI3K Akt signaling pathway.

PKI-179 is a potent, orally active compound that functions as a dual PI3K mTOR inhibitor. It demonstrates IC50 values of 8 nM for PI3K-α, 24 nM for PI3K-β, 74 nM for PI3K-γ, 77 nM for PI3K-δ, and 0.42 nM for mTOR. Additionally, it is effective against E545K and H1047R mutations, with IC50s of 14 nM and 11 nM, respectively. In vivo studies have shown that PKI-179 possesses anti-tumor capabilities[1][2].

PKI-179 is an orally bioavailable dual inhibitor of PI3K and mammalian target of rapamycin (mTOR). In an in vitro enzymatic assay, it potently inhibits PI3K (IC50s = 8, 24, 17, and 74 nM for isoforms α, β, δ, and γ, respectively), two common PI3Kα mutants, E545K and H1047R (IC50s = 14 and 11 nM, respectively), and mTOR (IC50 = 0.42 nM). PKI-179 is selective for PI3K and mTOR over a panel of 361 other kinases at IC50 values up to 50 μM, hERG (IC50 > 30 μM), and cytochrome P450 (CYP) isoforms (IC50s > 30 μM), but does have activity for CYP2C8 (IC50 = 3 μM). It inhibits proliferation through the Akt/mTOR signaling pathway in MDA-361 breast and PC3MM2 prostate cancer cell lines in vitro (IC50s = 22 and 29 nM, respectively) and inhibits tumor growth in an MDA-361 mouse xenograft model when used at a dose of 50 mg/kg.

1. β,β-Dimethylacrylshikonin (Dimethylacrylshikonin) is a promising agent for developing an improved strategy for radiotherapy against tumors. (a) Injection of Dimethylacrylshikonin combined with IR treatment significantly suppressed tumor growth of the HCT-116 xenograft. (b) Dimethylacrylshikonin significantly suppressed the growth of H(22) transplantable hepatoma, and induced the activation of caspase-3 . (c) Dimethylacrylshikonin inhibited growth of gastric cancer SGC-791 cells by inducing ERK signaling pathway. 2. Dimethylacrylshikonin inhibits the proliferation of MCF-7 cells in vitro by inducing apoptosis through the downregulation of Bcl-2, upregulation of Bax and partial inactivation of the NF-κB pathway.

Ac2-26, an annexin A1 mimetic peptide, was able to attenuate renal inflammatory injury in a diabetic mouse model through inhibition of p38MAPK NF-κB, as well as sepsis-induced cardiomyocyte apoptosis through the LXA4 PI3K AKT signalling pathway, and hepatic ischaemia-reperfusion injury in mice by modulating IL-22 IL-22R1 STAT3 signalling pathway.