19 Results for "

PI3K/AKT signaling axis

" in MedChemExpress (MCE) Product Catalog:
Products (19)

19 Results for "PI3K/AKT signaling axis" in MCE Product Catalog:

6
6 Publications Verification
Cat. No.: HY-113308
CAS No.: 516-90-5
Purity:  98.06%
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 (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 .
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6
6 Publications Verification
Cat. No.: HY-113308A
CAS No.: 6042-32-6
Purity:  99.81%
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 .
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2
2 Cited Publications
Cat. No.: HY-P99463
CAS No.: 2268717-61-7
Synonyms: AVB-500; AVB-S6-500

Research Areas:  

Cancer

Batiraxcept (AVB-500; AVB-S6-500) is a selective, soluble AXL receptor and GAS6 inhibitor that targets the GAS6-AXL signaling axis. Batiraxcept is orally inactive and does not cross the blood-brain barrier. Batiraxcept competitively binds to GAS6 ((KD <1 nM), preventing its interaction with the AXL receptor tyrosine kinase, thereby inhibiting downstream PI3K/AKT and MAPK signaling pathways, reducing tumor cell glycolysis, angiogenesis, and metastatic potential. Batiraxcept has demonstrated antitumor activity in preclinical models of endometrial, cholangiocarcinoma, and ovarian cancer by inhibiting tumor growth, invasion, and metastasis .
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1
1 Cited Publications
Cat. No.: HY-113308S1
CAS No.: 2410279-96-6
Taurolithocholic acid-d4 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 .
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1
1 Cited Publications
Cat. No.: HY-113308AS
CAS No.: 2410279-97-7
Purity:  99.4%
Taurolithocholic acid-d4 (sodium) is the deuterium labeled Taurolithocholic acid (sodium salt). 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 .
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Cat. No.: HY-N1255
CAS No.: 6451-73-6
Synonyms: (-)-Scoulerine; Discretamine
Scoulerine ((-)-Scoulerine; Discretamine) hydrochloride is a multi-target inhibitor with anti-tumor and antioxidant activities. Scoulerine mainly targets the PI3K/Akt/mTOR signaling axis and α1D-adrenergic receptor, disrupts microtubule structure, and induces cell cycle arrest and apoptosis. Scoulerine effectively inhibits mitochondrial dehydrogenase activity, targets GABA receptors and BACE1, and suppresses the proliferation, migration, invasion, epithelial-mesenchymal transition and stem cell properties of cancer cells. Scoulerine also exhibits multiple pharmacological activities including anti-Plasmodium falciparum, antibacterial, antiemetic and antitussive effects, and regulates endoplasmic reticulum stress and mitochondrial function (modulates Bax, Bcl-2 and cytochrome c). Scoulerine is applicable to research related to leukemia, ovarian cancer, and colorectal cancer .
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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 .
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Cat. No.: HY-174976
CAS No.: 3076057-63-8
FHND5032 is an orally active miR-124 inducer. FHND5032 significantly upregulates miR-124 expression in macrophages. FHND5032 disrupts inflammatory signaling, promotes macrophage reprogramming, and restores the epithelial barrier function by inhibiting the PIK3R2/PI3K/Akt axis. FHND5032 alleviates colitis and reduces inflammatory burden in ulcerative colitis mice. FHND5032 can be used for the study of ulcerative colitis .
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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-113308AR
CAS No.: 6042-32-6
Taurolithocholic acid (sodium salt) (Standard) is the analytical standard of Taurolithocholic acid (sodium salt). This product is intended for research and analytical applications. 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 .
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Cat. No.: HY-P990248
Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) is an anti-mouse E-Cadherin/CD324 IgG1 monoclonal antibody. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can downregulate the HER signaling axis and PI3K/Akt/mTOR signaling pathway. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can inhibit the proliferation of tumor cells and induce their apoptosis. Anti-Mouse E-Cadherin/CD324 Antibody (DECMA-1) can be used for researches on cancer and inflammation conditions such as breast cancer, chronic compression injury (CCI) and asthma .
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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 .
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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 .
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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 .
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Cat. No.: HY-183316
Research Areas:  

Cancer

Anticancer agent 319 is an anticancer agent. Anticancer agent 319 inhibits the proliferation of liver cancer cells. Anticancer agent 319 inhibits AKT phosphorylation and blocks the PI3K/AKT signaling axis; meanwhile, it inhibits ERK1/2 phosphorylation and blocks the MAPK/ERK signaling axis. Anticancer agent 319 induces G2/M phase cell cycle arrest, triggers apoptosis, and reduces mitochondrial membrane potential in liver cancer cells. Anticancer agent 319 can be used for the research of hepatocellular carcinoma .
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Cat. No.: HY-184303
Antihypertensive agent 7 is a vasodilator. Antihypertensive agent 7 acts on vascular endothelial cells to activate the PI3K/AKT signaling axis, increase phosphorylated eNOS, release NO, activate the sGC/cGMP pathway in smooth muscle cells, and synergistically activate multiple K + channels in vascular smooth muscle (Kir/Kv/KCa/KATP, thereby inducing endothelium-dependent vasodilation. Antihypertensive agent 7 can be used in the research of hypertension .
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Cat. No.: HY-179498
ROCK2-IN-13 is a selective ROCK2 inhibitor. ROCK2-IN-13 reduces nuclear expression by disrupting the interaction of ROCK2 with transcriptional co activators p300> and PGC 1α, repressing oncogenic transcription. ROCK2-IN-13 activates FOXO1 driven PTEN expression, leading to suppression of the PI3K/Akt pathway, induction of G2/M cell cycle arrest, and promotion of apoptosis. ROCK2-IN-13 ablates the nuclear transcriptional function of ROCK2 that sustains oncogenic signaling and restores the tumor suppressive PTEN/FOXO1 axis. ROCK2-IN-13 can be used for prostate cancer reseach .
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Cat. No.: HY-N1255A
CAS No.: 51486-68-1
Synonyms: (-)-Scoulerine hydrochloride; Discretamine hydrochloride
Scoulerine ((-)-Scoulerine; Discretamine) hydrochloride is a multi-target inhibitor with anti-tumor and antioxidant activities. Scoulerine hydrochloride mainly targets the PI3K/Akt/mTOR signaling axis and α1D-adrenergic receptor, disrupts microtubule structure, and induces cell cycle arrest and apoptosis. Scoulerine hydrochloride effectively inhibits mitochondrial dehydrogenase activity, targets GABA receptors and BACE1, and suppresses the proliferation, migration, invasion, epithelial-mesenchymal transition and stem cell properties of cancer cells. Scoulerine hydrochloride also exhibits multiple pharmacological activities including anti-Plasmodium falciparum, antibacterial, antiemetic and antitussive effects, and regulates endoplasmic reticulum stress and mitochondrial function (modulates Bax, Bcl-2 and cytochrome c). Scoulerine hydrochloride is applicable to research related to leukemia, ovarian cancer, and colorectal cancer .
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Cat. No.: HY-L249
6,182 compounds

Protein lactylation, an emerging post-translational modification identified in recent years, plays a critical role in linking cellular metabolic reprogramming, epigenetic regulation, and signaling networks. Based on a systematic framework encompassing lactate metabolism, lactylation, and downstream signaling pathways, this compound library comprehensively targets multiple regulatory layers, including histone modification enzymes (such as p300 and HDACs), key glycolytic enzymes (such as PKM2, LDHA, and GAPDH), transcriptional regulators (such as STAT3, HMGB1, and p53), as well as central signaling pathway nodes including HIF-1α, NF-κB, and PI3K-AKT-mTOR. This integrated design enables a comprehensive representation of the regulatory roles of lactylation across the “metabolism–epigenetics–signalingaxis.

MCE has assembled a collection of 6,182 known bioactive compounds and potential functional molecules, making this library suitable for a wide range of applications, including high-throughput drug screening, inhibitor identification, and mechanistic studies. It can be used to systematically evaluate the functional roles of lactylation in biological processes such as tumor metabolism, immune regulation, and inflammatory responses, and to efficiently identify small-molecule candidates with regulatory potential, thereby facilitating the development of innovative therapeutics targeting the interplay between metabolism and epigenetic regulation.

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