akt in 3

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

PI3K/Akt/mTOR-IN-2 is a potent PI3K/AKT/mTOR inhibitor with anticancer effects and selectivity for MDA-MB-231 cells (IC50 2.29 μM). It induces cell cycle arrest and apoptosis in cancer cells.

Akt3 degrader 1 is a specific Akt3 degrader with anticancer and antiproliferative activity that inhibits tumor growth in mice.Akt3 degrader 1 is used in the study of non-small cell lung cancer and pancreatic cancer.

STAT3/AKT-IN-1 is a dual inhibitor of the signal transducer and activator of transcription 3 (STAT3) and protein kinase B (AKT) signaling pathways, demonstrating anti-tumor activity and inducing apoptosis in SGC-7901 cells.

PI3K/AKT-IN-1 is a dual PI3K and AKT inhibitor with anti-cancer activity. It inhibits PI3Kγ, PI3Kδ, and AKT, suppressing the PI3K/AKT pathway and inducing caspase 3-dependent apoptosis, suitable for cancer research.

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.

PI3K/AKT-IN-4 (compound 3), a diterpenoid extracted from the roots and rhizomes of Salvia castanea Dielsf., exhibits antitumor properties by inhibiting cell viability and proliferation (IC 50 =4.72 μM) and promoting apoptosis in Hep3B cells. This compound obstructs the G0/G1 phase of the cell cycle, triggers mitochondrial dysfunction, and induces oxidative stress. Moreover, PI3K/AKT-IN-4 combats hepatocellular carcinoma through the inhibition of the PI3K-Akt signaling pathway and by interacting with PARP1 and CDK2 targets.

ALK/PI3K/AKT-IN-1 (Compound 45) effectively inhibits the proliferation of cancer cell lines A549, H1975, and PC9, with IC50 values of 0.44, 0.83, and 1.51 μM, respectively. This compound enhances the expression of p21 and p27, and decreases the activity of CDK2 and p-Rb, causing cell cycle arrest at the G1 phase. It suppresses the ALK/PI3K/AKT signaling pathway, promotes mitochondrial membrane potential depolarization, and induces apoptosis in A549 cells. Furthermore, ALK/PI3K/AKT-IN-1 inhibits the formation and growth of A549 cell spheres.

PI3K/Akt/mTOR-IN-4 (compound 4r) is a potent inhibitor targeting PI3K/Akt/mTOR pathways and tubulin polymerization. It induces apoptosis and causes cell cycle arrest at the G2/M phase. Additionally, PI3K/Akt/mTOR-IN-4 reduces the expression of p-PI3K, p-Akt, p-mTOR, and β-tubulin.

PI3K/Akt/mTOR-IN-6 (Compound JW4) is an orally active inhibitor of the PI3K/Akt/mTOR pathway. It induces apoptosis through the mitochondrial pathway and demonstrates significant anti-non-small cell lung cancer activity.

Akt3ligand-1 is an inhibitor of Akt3 with an IC50 of 0.1 nM and serves as a ligand for the PROTAC target protein (Akt3). It is utilized in the synthesis of PROTACAkt3Degrader-1.

PROTACAkt3Degrader-1 is an effective and selective PROTAC degrader targeting Akt3. It exhibits relatively weak antiproliferative activity across 36 cell lines. PROTACAkt3Degrader-1 is applicable in research on triple-negative breast cancer and melanoma.

PI3K/AKT/ERK/CREB activator 1 is an orally active agent that stimulates the PI3K/AKT/ERK/CREB signaling pathway. It supports neuronal survival and function, enhances neuron proliferation, and revives the activity of damaged neurons, while also aiding in synapse formation. By reducing pro-inflammatory cytokine levels, it alleviates neuroinflammation and preserves synaptic ultrastructure, thereby restoring spatial memory in Alzheimer's disease models. PI3K/AKT/ERK/CREB activator 1 serves as a valuable tool for Alzheimer's disease research.

PI3K/AKT-IN-6 is an orally active inhibitor of the PI3K/AKT signaling pathway and acts as an anti-inflammatory agent. It suppresses the production of pro-inflammatory cytokines TNF-α and IL-6, while reducing the expression of inflammatory mediators COX-2 and iNOS. PI3K/AKT-IN-6 alleviates symptoms in mouse models of colitis and can be used in research on inflammatory diseases such as colitis.

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

PI3K/Akt/CREB activator 1 (AE-18) is a selective inducible nitric oxide synthase (iNOS) inhibitor that crosses the blood-brain barrier, reduces infarct size and restores blood supply deficits after ischemia-reperfusion in rats, and is used in studies of vascular dementia and Parkinson's disease.

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.

Akt1-IN-3 (Compd 7) serves as an AKT1 inhibitor, specifically targeting AKT1-E17K with an IC50 of less than 15 nM [1].

PI3K/Akt/mTOR-IN-5 (compound D3), a derivative of Pseudolaric Acid B, exhibits antitumor activity. This compound inhibits excessive proliferation of tumor cells through the PI3K/AKT/mTOR and STAT3/GPX4 pathways. Additionally, PI3K/Akt/mTOR-IN-5 effectively suppresses the EDU positive rate, reduces colony formation, and induces apoptosis (apoptosis) by arresting HCT-116 cells in the S and G2/M phases.

Polyphyllin D induces apoptosis via the mitochondrial apoptotic pathway as evidenced by decreased Bcl-2 expression levels, disruption of MMP and increased Bax, cytochrome C, and cleaved-caspase-3 levels. Polyphyllin D has an anti-angiogenic effect. Polyphyllin D has toxicity in human RBCs as well as its underlying mechanism for the hemolysis and eryptosis/erythroptosis. Polyphyllin D has strong anticancer activity, can overcome drug resistance in R-HepG2 cells and elicit programmed cell death via mitochondrial dysfunction.

4-Vinylcyclohexene Dioxide (VCD) is an industrial epoxy resin intermediate and metabolite that exhibits a highly selective destructive effect on oocytes in primordial and primary follicles; it is used as a key inducer for establishing animal models of premature ovarian failure and premenopause. 4-Vinylcyclohexene Dioxide exerts its ovarian toxicity by activating caspase-dependent apoptotic pathways and can induce apoptosis in ovarian granulosa cells by upregulating reactive oxygen species and activating the PI3K/Akt/mTOR signaling pathway. It is used in reproductive toxicology and endocrine regulation research.

The combination of Valproic acid with Coumarin-3-carboxylic acid (3-Carboxycoumarin) suppresses the proliferation and migration of lung cancer cells via EGFR/VEGFR2/c-Met-Akt-NF-κB signaling pathways; this combination may have a wide therapeutic and/or adjuvant therapeutic application in the treatment of lung cancer.

ethyl 2-[3,5-bis(trifluoromethyl)phenyl]-3-oxo-2,3-dihydro-1H-pyrazole-4-carboxylate is a synthetic compound belonging to the curcumin family. It is involved in the regulation of immune response and inflammation through inhibition of the NF-κB signaling pathway, in the regulation of antioxidant response through activation of the Nrf2 signaling pathway, and in the regulation of cell survival and proliferation through inhibition of the Akt signaling pathway.

CAY10404 (3-(4-METHYLSULPHONYLPHENYL)-4-PHENYL-5-T) is a potent and highly selective inhibitor of COX-2 and COX-1. It is also a potent inhibitor of PKB/Akt and MAPK signalling pathways and induces apoptosis in NSC-LC cells, with analgesic, anti-inflammatory and anti-cancer activities.