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.

PI3Kδ-IN-22 (Compound 26) is a selective inhibitor of PI3Kδ with a pKi value of 9.3. It effectively inhibits the PI3Kδ-AKT signaling pathway in THP-1 cells, demonstrating a pIC50 of 9.4. Additionally, PI3Kδ-IN-22 exhibits favorable pharmacokinetic properties in rats.

PI3Kα-IN-22 (Compound 17) is a potent, selective, and orally active inhibitor targeting the PI3Kα H1047R mutation, exhibiting an IC 50 of 1 nM in the pAKT T47D AlphaLISA assay. It has demonstrated the ability to induce tumor regressions in the HCC1954 tumor model in mice [1].

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 hydrochloride is a potent and orally available dual PI3K/mTOR inhibitor. Its IC₅₀ values against PI3K-α, PI3K-β, PI3K-γ, PI3K-δ and mTOR are 8 nM, 24 nM, 74 nM, 77 nM and 0.42 nM respectively. It also exerts inhibitory activity against E545K and H1047R mutants with IC₅₀ values of 14 nM and 11 nM, and exhibits significant antitumor effects in in vivo models.

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.