pi3k-in-9

PI3K-IN-9 is a potent and selective inhibitor of PI3Kδ(IC50 of 8.9 nM).

Ethyl gallate (gallic acid ethyl ester) obviously decreases cell proliferation in MDA-MB-231 and MCF-7 cells in a dose- and time-dependent manner, exhibits cytotoxicity in a dose-dependent manner. Ethyl gallate can inhibit the abilities of invasion of breast cancer in vitro by inhibiting the mRNA levels of MMP-9/MMP-2, phosphorylation of Akt and protein expression of NF-κB and inhibits hydrogen peroxide signaling, may represent an alternative class of vasopressors for use in septic shock. Also, Ethyl gallate suppresses proliferation and invasion in human breast cancer cells by modulating the PI3K/Akt pathway, which may contribute to inhibiting their downstream targets such as NF-κB p-65, Bcl-2/Bax, and mRNA levels of MMP-2 and MMP-9 in breast cancer cells, could be used as potential antioxidants with safe therapeutic application in cancer chemotherapy.

Fusaric acid is an orally active multi-target inhibitor capable of inhibiting fibrosis-related signaling pathways such as NF-κB, TGF-β1/SMADs, and PI3K/AKT/mTOR. It also inhibits dopamine β-hydroxylase and reduces endogenous levels of norepinephrine and epinephrine. Fusaric acid activates apoptosis-related proteases such as Caspase-3/7, Caspase-8, and Caspase-9, thereby inducing oxidative stress and apoptosis. It chelates divalent metal cations, damages mitochondrial membrane structure, and exerts effects in improving myocardial fibrosis and alleviating cardiac hypertrophy. Additionally, it is applicable in research on esophageal cancer, liver cancer, and other conditions.

PI4KIIIbeta-IN-9 is a potent inhibitor of PI4KIIIβ [IC50 of 7 nM].

Rigosertib (ON-01910) is a selective, non-ATP-competitive PLK1 inhibitor (IC50: 9 nM) and multi-kinase inhibitor. As a selective anti-cancer agent, Rigosertib induces apoptosis by inhibiting the PI3 kinase/Akt pathway, promotes histone H2AX phosphorylation, and induces G2/M arrest in the cell cycle.

NF-κB-IN-16 (compound 9) is a complex of an NF-κB inhibitor and Cisplatin (Pt(IV) complex) with potent and low-toxicity antitumor activity. It can cause DNA damage, induce mitochondrial dysfunction, generate reactive oxygen species, and trigger apoptosis via mitochondrial pathways and endoplasmic reticulum stress. NF-κB-IN-16 effectively inhibits the NF-κB/MAPK signaling pathway and disrupts PI3K/AKT signal transduction. Additionally, it demonstrates excellent in vivo antitumor efficacy and low toxicity in A549 or A549/CDDP xenograft models.

PI3K/mTOR-IN-17 is a dual inhibitor that targets both PI3K and mTOR, with IC50 values of 1.21 μM and 0.21 μM, respectively. It induces apoptosis mediated by caspases and arrests cell growth in the G1 phase. The compound elevates the levels of caspases-3, 7, 8, and 9, enhances p53 expression, and increases the Bax/Bcl-2 ratio. By inhibiting the PI3K/mTOR signaling pathway, PI3K/mTOR-IN-17 is applicable in cancer research, including studies on non-small cell lung cancer (NSCLC).

ALR2-IN-9 is a potent inhibitor of ALR2 with an IC50 of 21.8 nM, demonstrating excellent antioxidant activity with an EC50 of 2.8 μM in DPPH free radical scavenging. It directly interacts with reactive oxygen (ROS) and reactive nitrogen species (RNS), blocking free radical chain reactions, and acts as an endogenous enzyme antioxidant regulator to modulate catalase (CAT) and superoxide dismutase (SOD) enzyme functions. By influencing the PI3K/Akt/Nrf2 pathway, ALR2-IN-9 inhibits excessive mitochondrial superoxide production induced by hyperglycemia in vitro and ameliorates oxidative stress induced by CuSO4 and H2O2 in vivo models. The compound also extends the lifespan of *Caenorhabditis elegans* by regulating stress response genes such as PMK-1 and shows potential as an anti-aging candidate. ALR2-IN-9 can be utilized in diabetes complication research.

EGFR-IN-182 (Compound 4) is an EGFR inhibitor with an IC50 value of 199 nM. It additionally inhibits HSP90 and PI3K, with IC50 values of 5.007 μM and 13.596 μM, respectively. EGFR-IN-182 demonstrates potent antiproliferative activity against MCF-7 and MDA-MB-231 cells. It downregulates Cyclin D1, induces cell cycle arrest, enhances caspase-9 activity, and triggers apoptosis. EGFR-IN-182 also decreases the expression of ERK and AKT and is applicable for breast cancer research.

SF2523 is a highly selective and potent inhibitor (SF2523) with improved physicochemical properties, excellent aqueous solubility, and biological efficacy. It is typically used in genome editing [CRISPR/Cas Solution] technology and can effectively enhance the efficiency of this process.

ON-01910 is a non-ATP-competitive PLK1 inhibitor(IC50 of 9 nM, in a cell-free assay). It shows 30-fold greater selectivity against Plk2 and no activity to Plk3. Rigosertib inhibits PI3K/Akt pathway and activates oxidative stress signals. Rigosertib induces apoptosis in various cancer cells.It is a synthetic benzyl styryl sulfone analogue with potential antineoplastic activity.

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

AKT-IN-9, a potent inhibitor of AKT, holds potential for breast and prostate cancer research.

1. 6-Shogaol (6-Shogaol) has antipyretic and analgesic effects in addition to inhibitory effect on lipoxygenase activity. 2. 6-shogaol has anti-inflammatory property, reduces the inflammatory response and protected the femoral cartilage from damage produced in a CFA monoarthritic model of the knee joint of rats. 3. 6-Shogaol inhibits the growth of human cancer cells and induces apoptosis in COLO 25 cells through modulation of mitochondrial functions regulated by reactive oxygen species (ROS). 4. 6-Shogaol effectively inhibit invasion and metastasis of hepatocellular carcinoma through diverse molecular mechanisms, including inhibition of the MAPK and PI3k/Akt pathways and NF-κB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis, could further regulate urokinase-type plasminogen activity.

Shogaol (Standard) is a reference standard for research and analysis in studies involving Shogaol. 1. 6-Shogaol (6-Shogaol) has antipyretic and analgesic effects in addition to inhibitory effect on lipoxygenase activity. 2. 6-shogaol has anti-inflammatory property, reduces the inflammatory response and protected the femoral cartilage from damage produced in a CFA monoarthritic model of the knee joint of rats. 3. 6-Shogaol inhibits the growth of human cancer cells and induces apoptosis in COLO 25 cells through modulation of mitochondrial functions regulated by reactive oxygen species (ROS). 4. 6-Shogaol effectively inhibit invasion and metastasis of hepatocellular carcinoma through diverse molecular mechanisms, including inhibition of the MAPK and PI3k/Akt pathways and NF-κB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis, could further regulate urokinase-type plasminogen activity.

Ethyl gallate (Standard) is a reference standard for research and analysis in studies involving Ethyl gallate. Ethyl gallate (gallic acid ethyl ester) obviously decreases cell proliferation in MDA-MB-231 and MCF-7 cells in a dose- and time-dependent manner, exhibits cytotoxicity in a dose-dependent manner. Ethyl gallate can inhibit the abilities of invasion of breast cancer in vitro by inhibiting the mRNA levels of MMP-9/MMP-2, phosphorylation of Akt and protein expression of NF-κB and inhibits hydrogen peroxide signaling, may represent an alternative class of vasopressors for use in septic shock. Also, Ethyl gallate suppresses proliferation and invasion in human breast cancer cells by modulating the PI3K/Akt pathway, which may contribute to inhibiting their downstream targets such as NF-κB p-65, Bcl-2/Bax, and mRNA levels of MMP-2 and MMP-9 in breast cancer cells, could be used as potential antioxidants with safe therapeutic application in cancer chemotherapy.

Euphorbia factor L1 (Standard) is a reference standard for research and analysis in studies involving Euphorbia factor L1. Euphorbia factor L1 (Euphorbiasteroid) can reduce Bcl-2, PI3K, AKT, and mTOR protein and mRNA levels, and up-regulate caspase-9 and caspase-3 protein levels. It induces autophagy and has anti-cancer, anti-adipogenic, anti-osteoclastogenic, and multidrug-resistant regulatory effects.

Cajanol is an isoflavanone isolated from the roots of pigeon pea [Cajanus cajan (L.) Millsp.]. It inhibits cancer cell proliferation and induces apoptosis. Cajanol increases Bax expression, inhibits Bcl-2 expression, activates caspase-9 and caspase-3, induces PARP cleavage, arrests the cell cycle at the G2/M phase, generates ROS, disrupts mitochondrial membrane potential, and triggers cytochrome c release. Additionally, cajanol induces bacterial DNA damage, disrupts bacterial cell membranes, and exhibits antibacterial activity in vitro. It reduces PI3K expression, inhibits Akt and NF-κB phosphorylation, downregulates P-gp expression and transport function, restores sensitivity of resistant cancer cells to Paclitaxel, and suppresses the growth of Paclitaxel-resistant metastatic ovarian tumors. Cajanol is applicable in research related to breast cancer, ovarian cancer, and bacterial infections.

YVPGP is an oligopeptide extracted from Anthopleura anjunae. It exhibits significant anti-tumor activity by mediating the PI3K/AKT/mTOR signaling pathway. YVPGP can arrest DU-145 cells in the S phase and induce apoptosis (apoptosis) through mitochondrial and death receptor pathways (caspase3, 7, 8, 9). It effectively inhibits tumor growth in a DU-145 xenograft mouse model, showing potential for prostate cancer research.