1309 Results for "

PI3K,

" in MedChemExpress (MCE) Product Catalog:
Products (1309)

1309 Results for "PI3K," in MCE Product Catalog:

Cat. No.: HY-Y1322
CAS No.: 115-86-6
Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring [3] .
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Cat. No.: HY-Y1322S
CAS No.: 1173020-30-8
Synonyms: Celluflex TPP-d15; DHPF 005-d15; Disflamol TP-d15; Disflamoll TP-d15; NSC 57868-d15; Phenyl phosphate ((PhO)3PO)-d15; Phoscon FR 903N-d15
Triphenyl phosphate-d15 is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.
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Cat. No.: HY-L125
2,810 compounds

Pulmonary fibrosis (PF), also known as diffuse interstitial pulmonary fibrosis, is a very common end-stage manifestation of several diseases, including idiopathic pulmonary fibrosis (IPF), pulmonary hypertension, and scleroderma, characterised by excessive matrix deposition and destruction of the lung architecture, finally leading to respiratory insufficiency. PF has become a global disease with significantly increased incidence rate, and the most common form of pulmonary fibrosis is idiopathic pulmonary fibrosis (IPF).

Lung fibrosis is a complex disease, a multitude of signal factors and signaling pathways is disrupted in this complex disease, such as TGF-β, Wnt, VEGF and PI3K–Akt. MCE offers a unique collection of 2,810 compounds with identified and potential anti-pulmonary fibrosis activity. MCE Anti-Pulmonary Fibrosis Compound Library is a useful tool for anti-pulmonary fibrosis drugs screening and other related research.

Cat. No.: HY-10201S4
CAS No.: 1333386-17-6
Synonyms: Donafenib tosylate; Bay 43-9006-d3 tosylate
Sorafenib-d3 (Donafenib) tosylate is the deuterated-labeled Sorafenib tosylate (HY-10201A). Sorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma [3] .
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Cat. No.: HY-113308AS1
CAS No.: 1265476-97-8
Taurolithocholic Acid-d5 (sodium) is the deuterium labeled Taurolithocholic acid sodium salt. Taurolithocholic Acid sodium salt is an orally active bile acid and antiviral agent. Taurolithocholic Acid sodium salt upregulates FADS2 by activating the TGR5-PI3K/AKT-SREBP2 signaling axis, inhibits SFTSV-induced ferroptosis, viral replication and viral entry of HBV/HDV, while reducing the release of IL-1β, lipid ROS and LDH. While exerting antiviral protective effects, Taurolithocholic Acid sodium salt also stimulates the recycling of hepatocellular membrane transporters, impairs canalicular bile acid secretion function, and induces hepatocyte cholestasis, apoptosis and acute hepatocellular injury. Taurolithocholic Acid sodium salt serves as an experimental model compound for hepatocellular cholestasis. At concentrations ≤200 μM, Taurolithocholic Acid sodium salt shows no cytotoxicity and does not activate the interferon pathway. Taurolithocholic Acid sodium salt not only protects mice from lethal SFTSV infection but also is suitable for studies related to severe fever with thrombocytopenia syndrome and cholestasis [3] .
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Cat. No.: HY-113308AS2
Taurolithocholic acid-d4-1 (sodium) is the deuterium labeled Taurolithocholic acid. Taurolithocholic acid sodium is an orally active bile acid and antiviral agent. Taurolithocholic acid sodium upregulates FADS2 by activating the TGR5-PI3K/AKT-SREBP2 signaling axis, inhibits SFTSV-induced ferroptosis, viral replication and viral entry of HBV/HDV, while reducing the release of IL-1β, lipid ROS and LDH. While exerting antiviral protective effects, Taurolithocholic acid sodium also stimulates the recycling of hepatocellular membrane transporters, impairs canalicular bile acid secretion function, and induces hepatocyte cholestasis, apoptosis and acute hepatocellular injury. Taurolithocholic acid sodium serves as an experimental model compound for hepatocellular cholestasis. At concentrations ≤200 μM, Taurolithocholic acid sodium shows no cytotoxicity and does not activate the interferon pathway. Taurolithocholic acid sodium not only protects mice from lethal SFTSV infection but also is suitable for studies related to severe fever with thrombocytopenia syndrome and cholestasis [3] .
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Cat. No.: HY-113308S
CAS No.: 1265681-64-8
Taurolithocholic acid-d5 is deuterium labeled Taurolithocholic acid. Taurolithocholic acid is an orally active bile acid and antiviral agent. Taurolithocholic acid upregulates FADS2 by activating the TGR5-PI3K/AKT-SREBP2 signaling axis, inhibits SFTSV-induced ferroptosis, viral replication and viral entry of HBV/HDV, while reducing the release of IL-1β, lipid ROS and LDH. While exerting antiviral protective effects, Taurolithocholic acid also stimulates the recycling of hepatocellular membrane transporters, impairs canalicular bile acid secretion function, and induces hepatocyte cholestasis, apoptosis and acute hepatocellular injury. Taurolithocholic acid serves as an experimental model compound for hepatocellular cholestasis. At concentrations ≤200 μM, Taurolithocholic acid shows no cytotoxicity and does not activate the interferon pathway. Taurolithocholic acid not only protects mice from lethal SFTSV infection but also is suitable for studies related to severe fever with thrombocytopenia syndrome and cholestasis [3] .
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Cat. No.: HY-114849R
CAS No.: 27314-13-2
Synonyms: SAN 9789 (Standard)
Norflurazon (Standard) (SAN 9789 (Standard)) is the analytical standard of Norflurazon (HY-114849). This product is intended for research and analytical applications. Norflurazon (SAN 9789) is a pre-emergence Herbicide. Norflurazon non-competitively inhibits phytoene desaturase by competing with the enzyme cofactor and disrupts carotenoid biosynthesis, thereby leading to chlorophyll photodegradation and chlorosis. Norflurazon inhibits MGDG synthase, CDP-choline phosphotransferase, Omega-3 FAD7 desaturase, and PG delta-3-trans desaturase, and activates LysoPC-acyltransferase and Omega-3 FAD3 desaturase. Norflurazon inhibits photosynthetic membrane organization, mitochondrial respiration, ATP production, PI3K signaling, and ERK1/2 phosphorylation. Norflurazon activates MAPK P38 phosphorylation and ER stress signaling. Norflurazon induces morphological malformations and cardiovascular effects in zebrafish embryos [3] .
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Cat. No.: HY-118160
CAS No.: 65240-86-0
Synonyms: NSC 73233
PPM-18 (NSC 73233) is a Vitamin K (HY-B2172) analog. PPM-18 prevents LPS-induced IκBα degradation, thereby inhibiting NF-κB activation and nuclear translocation of NF-κB. PPM-18 inhibits LPS-induced nitrite production and iNOS expression. PPM-18 inhibits HDAC6. PPM-18 induces ROS accumulation, activates AMPK, inhibits the mTORC1 and PI3K/AKT pathways, initiates Autophagy, and induces Apoptosis. PPM-18 suppresses seizures in zebrafish and mouse epilepsy models. PPM-18 prevents LPS-induced lethal toxicity and delayed hypotension. PPM-18 exhibits anticancer activity against leukemia and bladder cancer. PPM-18 can be used in research related to septic shock, bladder cancer and atherosclerosis [3].
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Cat. No.: HY-125101A
CAS No.: 1257792-42-9
Rafutrombopag (Hetrombopag) diolamine is an orally active nonpeptide thrombopoietin receptor (TPOR/MPL) agonist. Rafutrombopag diolamine can chelate iron and alleviate iron overload while promoting haematopoiesis. Rafutrombopag diolamine specifically stimulates proliferation and differentiation of human TPOR-expressing cells, including 32D-MPL and human hematopoietic stem cells through stimulation of STAT, PI3K and ERK signalling pathways. Rafutrombopag diolamine effectively up-regulates G1-phase-related proteins, including p-RB, Cyclin D1 and CDK4/6, normalizes progression of the cell cycle, and prevents apoptosis by modulating BCL-XL/BAK expression in 32D-MPL cells. Rafutrombopag diolamine protects cardiomyocyte survival from oxidative stress damage as an enhancer of stem cells. Rafutrombopag diolamine can be used for the study of immune thrombocytopenia and oxidative stress-related cardiovascular disease [3].
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Cat. No.: HY-128483R
CAS No.: 536-69-6
Fusaric acid (Standard) is the analytical standard of Fusaric acid (HY-128483). This product is intended for research and analytical applications. Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β1/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer [3] .
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Cat. No.: HY-175068
Synonyms: Ins(1,3,4,5,6)P5 sodium
Target:  

PI3K Akt Apoptosis

Research Areas:  

Cardiovascular Disease Cancer

D-myo-Inositol-1,3,4,5,6-pentaphosphate sodium (Ins(1,3,4,5,6)P5 sodium) is a small intracellular signaling molecule. D-myo-Inositol-1,3,4,5,6-pentaphosphate sodium inhibits the PI3K/Akt signaling pathway. D-myo-Inositol-1,3,4,5,6-pentaphosphate sodium inhibits Akt/PKB phosphorylation and kinase activity, inducing apoptosis in cancer cells. D-myo-Inositol-1,3,4,5,6-pentaphosphate sodium inhibits the formation of tubular structures in endothelial cells in an in vitro angiogenesis mouse model. D-myo-Inositol-1,3,4,5,6-pentaphosphate sodium can be used in research on ovarian cancer, lung cancer, breast cancer, and other cancers, as well as in cardiovascular and cerebrovascular diseases such as angiogenesis .
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Cat. No.: HY-18234B
CAS No.: 24365-47-7
Leupeptin Ac-LL is a broad-spectrum protease inhibitor . By inhibiting the activation of the PTEN/PI3K/Akt/NF-κB/ERK1/2/p38 signaling pathway, Leupeptin Ac-LL significantly reduces LPS-induced NO and ROS production, mitochondrial membrane potential hyperpolarization, phagocytic activity, pro-inflammatory cytokine release, and M1 polarization in mouse peritoneal macrophages, and reverses autophagic flux impairment. It also decreases Concanavalin A (HY-P2149)-induced proliferation index of mouse splenic lymphocytes and the Th1/IL-10 and Th2/IL-10 cytokine ratios, thereby modulating innate and adaptive immune responses. Leupeptin Ac-LL inhibits blood coagulation and tumorigenesis in mouse skin. Leupeptin Ac-LL can be used in research on chronic inflammatory diseases and skin tumorigenesis [3].
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Cat. No.: HY-18234C
CAS No.: 24125-16-4
Leupeptin Ac-LL hydrochloride is a broad-spectrum protease inhibitor . By inhibiting the activation of the PTEN/PI3K/Akt/NF-κB/ERK1/2/p38 signaling pathway, Leupeptin Ac-LL hydrochloride significantly reduces LPS-induced NO and ROS production, mitochondrial membrane potential hyperpolarization, phagocytic activity, pro-inflammatory cytokine release, and M1 polarization in mouse peritoneal macrophages, and reverses autophagic flux impairment. It also decreases Concanavalin A (HY-P2149)-induced proliferation index of mouse splenic lymphocytes and the Th1/IL-10 and Th2/IL-10 cytokine ratios, thereby modulating innate and adaptive immune responses. Leupeptin Ac-LL hydrochloride inhibits blood coagulation and tumorigenesis in mouse skin. Leupeptin Ac-LL hydrochloride can be used in research on chronic inflammatory diseases and skin tumorigenesis [3].
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Cat. No.: HY-B0633I
CAS No.: 9067-32-7
Hyaluronic acid sodium (MW 800kDa) is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid sodium is a major component of the extracellular matrix (ECM). Hyaluronic acid sodium is synthesized at the plasma membrane. Increased hyaluronic acid sodium levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid sodium participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid sodium activates the PI3K-Akt signaling. Hyaluronic acid sodium acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid sodium also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid sodium can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid sodium can be studied in joint diseases, wound healing and cancer [3] .
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Cat. No.: HY-B1203R
CAS No.: 127-31-1
Synonyms: 9α-Fludrocortisone (Standard); 9α-Fluorcortisol (Standard)
Fludrocortisone (Standard) (9α-Fludrocortisone (Standard)) is the analytical standard of Fludrocortisone (HY-B1203). This product is intended for research and analytical applications. Fludrocortisone is an orally active mineralocorticoid and glucocorticoid receptor agonist. Fludrocortisone suppresses pro-inflammatory cytokine expression, reduces CCL2, IL-6, IL-8 levels, upregulates mineralocorticoid receptor (MR) expression, induces PI3K/Akt, GSK-3β, CREB, ERK1/2, mTOR phosphorylation, blocks Tau hyperphosphorylation, prevents apoptosis, promotes survival and proliferation, enhances renal sodium and water transport, increases plasma volume and blood pressure, reduces plasma potassium and renin activity, stimulates erythropoietin expression, modulates uterine receptivity genes, and reverses PP242-induced MUC1 upregulation. Fludrocortisone can be used for the research of congenital adrenal hyperplasia, postural hypotension, and adrenal insufficiency.
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Cat. No.: HY-B1203S
Synonyms: 9α-Fludrocortisone-d5; 9α-Fluorcortisol-d5
Fludrocortisone-d5 (9α-Fludrocortisone-d5) is the deuterium labeled Fludrocortisone (HY-B1203). Fludrocortisone is an orally active mineralocorticoid and glucocorticoid receptor agonist. Fludrocortisone suppresses pro-inflammatory cytokine expression, reduces CCL2, IL-6, IL-8 levels, upregulates mineralocorticoid receptor (MR) expression, induces PI3K/Akt, GSK-3β, CREB, ERK1/2, mTOR phosphorylation, blocks Tau hyperphosphorylation, prevents apoptosis, promotes survival and proliferation, enhances renal sodium and water transport, increases plasma volume and blood pressure, reduces plasma potassium and renin activity, stimulates erythropoietin expression, modulates uterine receptivity genes, and reverses PP242-induced MUC1 upregulation. Fludrocortisone can be used for the research of congenital adrenal hyperplasia, postural hypotension, and adrenal insufficiency.
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Cat. No.: HY-B1203S1
Synonyms: 9α-Fludrocortisone-d2; 9α-Fluorcortisol-d2
Fludrocortisone-d2 (9α-Fludrocortisone-d2) is the deuterium labeled Fludrocortisone (HY-B1203). Fludrocortisone is an orally active mineralocorticoid and glucocorticoid receptor agonist. Fludrocortisone suppresses pro-inflammatory cytokine expression, reduces CCL2, IL-6, IL-8 levels, upregulates mineralocorticoid receptor (MR) expression, induces PI3K/Akt, GSK-3β, CREB, ERK1/2, mTOR phosphorylation, blocks Tau hyperphosphorylation, prevents apoptosis, promotes survival and proliferation, enhances renal sodium and water transport, increases plasma volume and blood pressure, reduces plasma potassium and renin activity, stimulates erythropoietin expression, modulates uterine receptivity genes, and reverses PP242-induced MUC1 upregulation. Fludrocortisone can be used for the research of congenital adrenal hyperplasia, postural hypotension, and adrenal insufficiency.
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Cat. No.: HY-G0007R
CAS No.: 88546-55-8
Synonyms: Omeprazole sulphone (Standard)
Omeprazole sulfone (Standard) is the analytical standard of Omeprazole sulfone. This product is intended for research and analytical applications. Omeprazole sulfone (Omeprazole sulphone) is one of the major circulating metabolites of Omeprazole (HY-B0113) in vivo, and belongs to class 4 non-mutagenic impurities. Omeprazole sulfone does not bind to the aryl hydrocarbon receptor (AhR), nor does it induce the expression of CYP1A1 or CYP1A2. However, Omeprazole sulfone promotes the migration of gastric epithelial cells under basal conditions and reverses the inhibitory effect of Indomethacin (HY-14397) on cell migration. Omeprazole sulfone does not promote cell proliferation, nor does it upregulate COX-2 expression or activate signaling pathways such as ERK, P38 MAPK and PI3K. Omeprazole sulfone maintains basal ulcer healing under non-acid-dependent conditions and can be used in studies related to gastric ulcer repair [3] .
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Cat. No.: HY-G0007S1
CAS No.: 1261393-28-5
Synonyms: Omeprazole sulfone-13C,d3; Omeprazole sulphone-13C,d3
Omeprazole sulfone- 13C,d3 is the deuterium and 13C labeled Omeprazole sulfone. Omeprazole sulfone (Omeprazole sulphone) is one of the major circulating metabolites of Omeprazole (HY-B0113) in vivo, and belongs to class 4 non-mutagenic impurities. Omeprazole sulfone does not bind to the aryl hydrocarbon receptor (AhR), nor does it induce the expression of CYP1A1 or CYP1A2. However, Omeprazole sulfone promotes the migration of gastric epithelial cells under basal conditions and reverses the inhibitory effect of Indomethacin (HY-14397) on cell migration. Omeprazole sulfone does not promote cell proliferation, nor does it upregulate COX-2 expression or activate signaling pathways such as ERK, P38 MAPK and PI3K. Omeprazole sulfone maintains basal ulcer healing under non-acid-dependent conditions and can be used in studies related to gastric ulcer repair [3].
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