pi3k in 10

PI3K-IN-10 is a potent inhibitor of pan-PI3K (Phosphoinositide 3-kinase).

PI3Kδ-IN-10 is a highly potent and orally active PI3Kδ inhibitor (IC50 = 2 nM) that robustly suppresses the downstream AKT pathway to induce subsequent apoptosis in hepatocellular carcinoma models.

ALK-IN-31 (Compound Ld-10) is an orally active ALK inhibitor with an IC50 of 1135 nM. It demonstrates excellent antiproliferative activity against lung cancer cells H2228, with an IC50 value of 1.35 μM. ALK-IN-31 induces apoptosis and arrests cell proliferation at the G0/G1 phase by affecting mitochondrial function. It exhibits antitumor effects by downregulating the expression of p-AKT and p-mTOR in the PI3K-AKT-mTOR signaling pathway downstream of ALK. This compound is applicable for research into non-small cell lung cancer (NSCLC).

PI3K-IN-23 is a (E)-9-oxooctadec-10-en-12-ynoic acid analogue that promotes glucose uptake (EC50: 7.00 μM).

AKT-IN-10 is a potent AKT inhibitor with research potential in breast and prostate cancers. It targets protein kinase B (PKB, also known as AKT), a key component of the PI3K/AKT/mTOR signaling pathway that is crucial for cell growth, survival, differentiation, and metabolism.

PI3K/mTOR Inhibitor-7 is a potent dual PI3K/mTOR inhibitor. PI3K/mTOR Inhibitor-7 is 4.7-fold more potent than gedatolisib, with IC50 values of 1.4 μM and 0.3 μM, respectively. 10 μM of PI3K/mTOR Inhibitor-7 is able to significantly inhibit the PI3K/Akt/mTOR signalling pathway. PI3K/mTOR Inhibitor-7 has shown potential for research in cancer diseases.

PI3K/mTOR Inhibitor-6 (Compound 19c) is a potent dual PI3K/mTOR inhibitor, exhibiting greater stability than gedatolisib in artificial gastric fluid. At 10 μM, PI3K/mTOR Inhibitor-6 significantly inhibits the PI3K/Akt/mTOR signaling pathway and has shown potential for cancer research.

PLM-101 is an anticancer compound orally active against acute myeloid leukemia by targeting FLT3 and RET. It impedes RET function, promoting autophagic breakdown of FLT3, and suppresses the PI3K and Ras/ERK pathways, contributing to its anti-leukemic effects. The compound's antitumor efficacy is demonstrated in both a mouse MV4-11 flank xenograft model (doses of 3 and 10 mg/kg; po) and an allogeneic xenograft mouse model (dose of 40 mg/kg; po) [1].

Compound F27 (Antileishmanial agent-19) is an antileishmanial compound effective against L. donovani promastigotes, demonstrating an IC50 of 3.39 μM. It functions by inhibiting the Leishmania prolyl-tRNA synthetase and disrupting the host PI3K/Akt/CREB axis-mediated IL-10 secretion. Additionally, Compound F27 promotes autophagy-mediated apoptosis in L. donovani promastigotes and has been shown to reduce parasite burden in L.d-infected animals [1].

PI3K-IN-51, characterized as a PI3K inhibitor, exhibits IC50 values below 500 nM for p120γ and p110δ/p85α (WO2016204429A1; Example 10) [1].

Antcin K is a selective inhibitor that targets the PI3K/Akt, NF-κB, MEK1/2-ERK, p38, and AP-1 pathways. It enhances IL-10 expression, thereby suppressing pro-inflammatory cytokine production, blocking monocyte adhesion, reducing tissue damage, and promoting myogenesis. Antcin K exhibits significant anti-inflammatory, anti-damage, and tissue-protective activities. It is primarily studied in the context of inflammatory-related diseases such as periodontitis, rheumatoid arthritis, and skeletal muscle injury.

Kushenol I is a bioactive compound exhibiting anti-inflammatory, antioxidant, and ulcerative colitis–ameliorating effects, demonstrated in a DSS-induced UC mouse model where oral administration improved colon length, body weight, and disease scores while reducing pro-inflammatory cytokines including IL-1β, IL-6, IL-17, and TNF-α. Kushenol I increase IL-10 expression, inhibited key inflammatory signaling proteins such as AKT, p38 MAPK, PI3K, NLRP3, FOXO1, and TLR4, enhancing intestinal barrier integrity. Kushenol I positively modulate gut microbiota, and elevated splenic T-cell proportions, supporting therapeutic potential in inflammatory bowel disease.