pi3k/akt/mtor. pathway

PI3K/Akt/mTOR-IN-2 is a potent PI3K/AKT/mTOR inhibitor.PI3K/Akt/mTOR-IN-2 has anticancer effects and is selective for MDA-MB-231 cells with an IC50 of 2.29 μM.PI3K/Akt/mTOR-IN-2 exhibits anticancer activity and induces cycle arrest and apoptosis in cancer cells. PI3K/Akt/mTOR-IN-2 has anticancer activity and can induce cycle arrest and apoptosis in cancer cells.

mTOR inhibitor-3 is a selective mTOR inhibitor (Ki= 1.5 nM). mTOR inhibitor-3 inhibits mTORC1 and mTORC2 in cellular and in vivo experiments.

PI3K/mTOR Inhibitor-14 (compound Y-2) serves as a dual inhibitor of PI3K and mTOR, exhibiting IC50 values of 171.4 nM and 10.1 nM , respectively, and demonstrates antitumor activities [1].

Wnt pathway inhibitor 3 is a potent AC1 inhibitor with an IC50 value of 45 nM.Wnt pathway inhibitor 3 has antiproliferative activity and can be used in studies to ameliorate osteoarthritis in a mouse model of experimental osteoarthritis.

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 that is more stable than gedatolisib in artificial gastric fluid. 10 μM of PI3K/mTOR Inhibitor-6 significantly inhibits the PI3K/Akt/mTOR signalling pathway. PI3K/mTOR Inhibitor-6 has shown potential for research in cancer diseases.

PI3K/mTOR Inhibitor-1 is a potent, orally bioavailable dual inhibitor of PI3K/mTOR (PI3Kα/PI3Kβ/PI3Kδ/PI3Kγ/mTOR with IC50s of 20/376/204/46/186 nM)

PI3K/mTOR Inhibitor-12, a potent and selective orally active inhibitor, exhibits IC50 values of 0.06 nM for PI3Kα and 3.12 nM for mTOR, indicating significant antitumor activity with reduced liver toxicity [1].

PI3K/AKT-IN-2, a dual inhibitor of PI3K and AKT, prevents the epithelial-mesenchymal transition (EMT) and promotes apoptosis. Additionally, it impedes tubulin polymerization.

PI3K/mTOR Inhibitor-3 (compound 12) is an imidazoline compound with potent dual inhibitory effects on PI3K and mTOR. This compound exhibits notable anti-cancer activity [1].

PI3K/Akt-IN-C89 is a novel Inhibitor of the PI3K-Akt Pathway, Inducing Autophagy of Female Germline Stem Cells.

PI3K/mTOR Inhibitor-4 is an orally active pan-I PI3K/mTOR inhibitor. PI3K/mTOR Inhibitor-4 is an enzyme inhibitor that acts on PI3Kα (IC50: 0.63 nM), PI3Kγ (IC50: 22 nM), PI3Kδ (IC50: 9.2 nM) and mTOR (IC50: 13.85 nM). PI3K/mTOR Inhibitor-4 can be used to study cancer.

Heterocyclic compounds as covalent inhibitors of G12C mutant K-Ras protein useful for treating cancers.K-Ras G12C-IN-3 is a novel and irreversible inhibitor of mutant K-ras G12C.

PI3K/Akt/CREB Activator 1 is a potent, orally active compound that acts as an activator for the PI3K/Akt/CREB pathway. It enhances neuronal proliferation, induces differentiation of Neuro-2a cells into neuron-like morphology, and accelerates axon-dendrite polarization in primary hippocampal neurons by upregulating brain-derived neurotrophic factor. This compound is utilized in vascular dementia (VaD) research.

Cathepsin K Inhibitor 3, exhibiting an IC50 value of 0.5 nM, is a highly selective inhibitor of cathepsin K, featuring a favorable pharmacokinetic profile. It holds potential for use in studies of osteoarthritis (OA).

PI3K/mTOR Inhibitor-8 is a dual inhibitor of PI3K (PI3Kα IC50: 0.46 nM) and mTOR (mTOR IC50: 12 nM). PI3K/mTOR Inhibitor-8 blocks the cell cycle of HCT-116 cells in G1/S phase and induces apoptosis. apoptosis).

K-Ras ligand-Linker Conjugate 3 (Compound 001371) is a chemical compound that consists of a ligand for K-Ras recruiting moiety and a PROTAC linker, responsible for recruiting E3 ligases (e.g., VHL, CRBN, MDM2, and IAP). This compound is essential in the synthesis of PROTAC K-Ras Degrader-1, a potent PROTAC K-Ras degrader that demonstrates a degradation efficacy of ≥70% in SW1573 cells[1].

PI3K/AKT-IN-1 is a potent, dual PI3K/AKT inhibitor that acts on PI3Kγ (IC50: 6.99 μM), PI3Kδ (IC50: 4.01 μM) and AKT (IC50: 3.36 μM). PI3K/AKT-IN-1 induces caspase 3-dependent apoptosis by inhibiting the PI3K/AKT pathway. caspase 3-dependent apoptosis and exhibited anticancer effects.

PI3K/mTOR Inhibitor-9 (Compound 1) is a potent inhibitor of both mTOR and PI3K, acting on mTOR (IC50: 38 nM), PI3Kα (IC50: 6.6 nM), PI3Kγ (IC50: 6.6 nM) and PI3Kδ (IC50: 0.8 nM).

PI3K/mTOR Inhibitor-2 is a potent pan inhibitor of PI3K and mTOR with IC50s of 3.4, 34, 16,1 and 4.7 nM for PI3Kα, PI3Kβ, PI3Kδ, PI3Kγ and mTOR. PI3K/mTOR Inhibitor-2 has antitumor activity.

K 259-3, a methyl ester of K 259-2, is an inhibitor of calmodulin-dependent cyclic nucleotide phosphodiesterase.

PI3K/mTOR Inhibitor-13, an orally active dual inhibitor targeting phosphoinositol 3-kinase (PI3K) and mTOR kinase, holds potential for treating sexual diseases, solid tumors, and idiopathic pulmonary fibrosis (IPF).

PI3K/mTOR Inhibitor-5 is a potent dual inhibitor of PI3K and mTOR, displaying IC50 values of 86.9 nM (for PI3K) and 14.6 nM (for mTOR), respectively.

PI3K/Akt/mTOR-IN-3 is a potent inhibitor of PI3K/Akt/mTOR. PI3K/Akt/mTOR-IN-3 inhibits the migration of MCF-7 cells (IC50: 0.77 μM), HeLa cells (IC50: 1.23 μM) and HepG2 cells (IC50: 4.57 μM). PI3K/Akt/mTOR-IN-3 inhibited the migration of MCF-7 and HeLa cells at a concentration of 4 μM. PI3K/Akt/mTOR-IN-3 blocked the cell cycle in S phase and induced apoptosis.

AKT-IN-3 is a potent, orally active low hERG blocking Akt inhibitor (IC50: 1.4 nM, 1.2 nM, and 1.7 nM for Akt1, Akt2, and Akt3). AKT-IN-3 (compound E22) also exhibits good inhibitory activity against other AGC family kinases, such as PKA, PKC, ROCK1, RSK1

Fimepinostat (CUDC 907) is an orally bioavailable inhibitor of both phosphoinositide 3-kinase (PI3K) class I and pan-histone deacetylase (HDAC) enzymes, with potential antineoplastic activity. Upon oral administration, CUDC-907 inhibits the activity of both PI3K class I isoforms and HDAC, thereby preventing the activation of the PI3K-AKT-mTOR signal transduction pathway that is often overactivated in many cancer cell types.

Ridaforolimus (AP23573) is a small molecule and non-prodrug analogue of the lipophilic macrolide antibiotic rapamycin with potential antitumor activity. Ridaforolimus binds to and inhibits the mammalian target of rapamycin (mTOR), which may result in cell cycle arrest and, consequently, the inhibition of tumor cell growth and proliferation. Upregulated in some tumors, mTOR is a serine/threonine kinase involved in regulating cellular proliferation, motility, and survival that is located downstream of the PI3K/Akt signaling pathway.

Arnicolide D is a sesquiterpene lactone. Arnicolide D isolates from Centipeda minima. Arnicolide D modulates the cell cycle, activates the caspase signaling pathway and inhibits the PI3K/AKT/mTOR and STAT3 signaling pathways. Arnicolide D inhibits Nasopharyngeal carcinoma (NPC) cell viability in a concentration- and time-dependent manner. Arnicolide D exerts strong cytotoxic activity on the human colon carcinoma HT-29 cell line.

Topoisomerase I/II inhibitor 3 (compound 7) is a potent dual inhibitor of topoisomerase I (Topo I) and II (Topo II) . By inhibiting PI3K /Akt/mTOR signaling pathway, Topoisomerase I/II inhibitor 3 can inhibit cell proliferation, invasion and migration, and induce apoptosis . Topoisomerase I/II inhibitor 3 has research value in liver cancer.

XC-302 is a multi-targeted inhibitor, it induces autophagy of nasopharyngeal cancer cells via inhibiting the PI3K/AKT/mTOR signaling pathway.

Antiproliferative agent-32 (Compound 1c) impedes phosphorylation within the PI3K/Akt/mTOR signaling pathway, restrains proliferation of Huh7 and SK-Hep-1 cells, induces apoptosis, and inflicts mitochondrial damage, rendering it a potential subject for hepatocellular carcinoma research [1].

Hederacolchiside A1 (Raddeanoside R13) shows anti-leishmanial activity, it exhibits a strong antiproliferative activity on all stages of development of the parasite by altering membrane integrity and potential. Hederacolchiside A1 shows antiproliferation activities in three cancer cell lines with the IC50 value of 2.4 uM, it exhibits a preferential cytotoxicity on a pigmented melanoma cell line. It suppresses proliferation of tumor cells by inducing apoptosis through modulating PI3K/Akt/mTOR signaling pathway.

Brevilin A is a sesquiterpene lactone isolated from Centipeda minima, inhibits janus kinase activity and blocks STAT3 signaling in cancer cells with anti-tumor activity. Brevilin A is a selective inhibitor of JAK-STAT signal pathway by attenuating the JAKs activity and blocking STAT3 signaling (IC50 = 10.6 μM) in Cancer Cells.Brevilin A induces apoptosis and autophagy via mitochondrial pathway and PI3K/AKT/mTOR inactivation in colon adenocarcinoma cell CT26.antitumour

HSP90/mTOR-IN-1 is an effective and orally administrable inhibitor targeting both Hsp90 and mTOR, displaying IC50 values of 69 nM and 29 nM, respectively. This compound inhibits the proliferation of SW780 cells by overly activating the PI3K/AKT/mTOR pathway and induces apoptosis and autophagy through its selective inhibition of Hsp90 and mTOR. Additionally, HSP90/mTOR-IN-1 exhibits significant anti-tumor activity in vivo and is applicable in bladder cancer research.

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.

AZD-3463 (ALK/IGF1R inhibitor) , an orally bioavailable ALK inhibitor (Ki: 0.75 nM), can inhibit IGF1R with equivalent potency.