Search Result
Results for "
PI3K/Akt/GSK3β
" in MedChemExpress (MCE) Product Catalog:
1
Biochemical Assay Reagents
2
Isotope-Labeled Compounds
| Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
-
- HY-15244
-
Alpelisib
Maximum Cited Publications
125 Publications Verification
BYL-719
|
PI3K
Apoptosis
|
Cancer
|
|
Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
|
-
-
- HY-B1203
-
|
9α-Fludrocortisone; 9α-Fluorcortisol
|
Mineralocorticoid Receptor
Glucocorticoid Receptor
Apoptosis
|
Neurological Disease
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
Fludrocortisone (9α-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 .
|
-
-
- HY-N0721
-
-
-
- HY-N0815
-
Resibufogenin
Maximum Cited Publications
7 Publications Verification
Bufogenin; Recibufogenin
|
PI3K
Akt
NF-κB
AP-1
GSK-3
CDK
|
Neurological Disease
Inflammation/Immunology
Cancer
|
|
Resibufogenin is an orally active anticancer agent. Resibufogenin can be extracted from toad venom. Resibufogenin blocks signaling pathways such as PI3K/Akt, NF-κB, AP-1, activates GSK-3β, and regulates cyclin D1. Resibufogenin can activate central neurons. Resibufogenin has anti-inflammatory activity. Resibufogenin has anti-tumor effects on a variety of tumors such as multiple myeloma, renal cancer, colorectal cancer, pancreatic cancer, and glioma .
|
-
-
- HY-125848
-
|
|
Apoptosis
AMPK
PPAR
p38 MAPK
PI3K
Akt
GSK-3
Reactive Oxygen Species (ROS)
SOD
Caspase
|
Neurological Disease
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota . Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma .
|
-
-
- HY-18676
-
|
|
Integrin
Autophagy
Apoptosis
|
Cancer
|
|
OSU-T315 (ILK-IN-1) is a small Integrin-linked kinase (ILK) inhibitor with an IC50 of 0.6 μM, inhibiting PI3K/AKT signaling by dephosphorylation of AKT-Ser473 and other ILK targets (GSK-3β and myosin light chain) . OSU-T315 abrogates AKT activation by impeding AKT localization in lipid rafts and triggers caspase-dependent apoptosis in an ILK-independent manner . OSU-T315 causes cell death through apoptosis and autophagy .
|
-
-
- HY-15244A
-
|
BYL-719 hydrochloride
|
PI3K
Apoptosis
|
Cancer
|
|
Alpelisib (BYL-719) hydrochloride is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib hydrochloride also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib hydrochloride not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib hydrochloride can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
|
-
-
- HY-15978
-
|
|
Others
|
Neurological Disease
|
|
P7C3-A20 is a derivative of P7C3 with potent proneurogenic and neuroprotective activity. P7C3-A20 exerts an antidepressant-like effect. P7C3-A20 can cross the blood-brain barrier and therefore has the potential for brain injury treatment .
|
-
-
- HY-N0695
-
|
Gomisin-B; Wuweizi ester-B; Schisantherin-B
|
PI3K
Akt
mTOR
GSK-3
Tau Protein
TNF Receptor
Interleukin Related
Apoptosis
|
Neurological Disease
Inflammation/Immunology
|
|
Schisantherin B (Gomisin-B) is a lignan compound and one of the active components of Schisandra chinensis. Schisantherin B activates the PI3K/AKT signaling pathway, restores the activity of GSK3β, and reduces the hyperphosphorylation of tau protein in hippocampal and cerebral cortical tissues. Schisantherin B upregulates the level of GLT-1, decreases the expression of pro-inflammatory cytokines TNF-α/IL-1β/IL-6, upregulates the expression of IL-10, and inhibits cell apoptosis. Schisantherin B is applicable to the research of spinal cord injury, Alzheimer's disease and depression .
|
-
-
- HY-N6064
-
|
|
Apoptosis
IAP
|
Cancer
|
|
Polygalacin D (PGD) is a bioactive compound isolated from Platycodon grandiflorum with anticancer and anti-proliferative properties.
PGD suppresses the expression of the IAP family of proteins including survivin, cIAP-1 and cIAP-2 and blocks the PI3K/Akt pathway by inhibiting the phosphorylation of GSK3β, Akt and the expression of PI3K. Polygalacin D induces apoptosis
|
-
-
- HY-N6580
-
-
-
- HY-P6292
-
|
|
PACAP Receptor
PKA
ERK
PI3K
Akt
GSK-3
|
Neurological Disease
Cancer
|
|
KS-133 is a bicyclic peptide with VIPR2 antagonistic activity that can cross the blood-brain barrier. KS-133 selectively blocks VIPR2-mediated Gq/Ca, Gs/cAMP, cAMP/PKA/ERK and PI3K/AKT/GSK3β signaling pathways. KS-133 inhibits VIPR2 agonist-induced CREB phosphorylation in the prefrontal cortex of mice. KS-133 shifts the polarization direction of macrophages toward M1. KS-133 attenuates cancer cell proliferation and reduces the cell cycle distribution level at the S-M phase. KS-133 exerts antitumor effects in a mouse model of colorectal cancer. KS-133 reverses cognitive decline in mouse models of psychiatric disorders. KS-133 can be used for research related to schizophrenia, colorectal cancer and breast cancer .
|
-
-
- HY-N7363
-
|
(-)-Isolongifolene
|
Environmental Pollutants
Apoptosis
|
Neurological Disease
Inflammation/Immunology
Cancer
|
|
Isolongifolene ((-)-Isolongifolene) is a tricyclic sesquiterpene isolated from Murraya koenigii. Isolongifolene attenuates Rotenone-induced oxidative stress, mitochondrial dysfunction and apoptosis through the regulation of PI3K/AKT/GSK-3β signaling pathways. Isolongifolene has antioxidant, anti-inflammatory, anticancer and neuroprotective properties .
|
-
-
- HY-126049
-
|
(S)-(-)-Oxiracetam; (S)-ISF2522
|
Apoptosis
|
Neurological Disease
|
|
(S)-oxiracetam (S-ORC) is an inhibitor targeting apoptosis. S-ORC reduces brain infarct size and lessens neurological dysfunction in middle cerebral artery occlusion/reperfusion (MCAO/R) models. S-ORC prevents neuronal apoptosis via activating PI3K/Akt/GSK3β signaling pathway via α7 nAChR after ischemic stroke. S-ORC can prevent neuronal death after ischemic stroke .
|
-
-
- HY-N0721R
-
-
-
- HY-P11313
-
|
Rat chromogranin A367–387
|
nAChR
Akt
|
Cardiovascular Disease
|
|
Catestatin (rat) (Rat chromogranin A367–387) is a potent, reversible, noncompetitive, and noncooperative nicotinic cholinergic antagonist derived from chromogranin A (A367-387). Catestatin (rat) inhibits norepinephrine release in rat PC12 pheochromocytoma cells (IC50 = 1.2 μM), and blocks desensitization of norepinephrine release (IC50 = 0.62 μM). Catestatin (rat) exerts antiadrenergic effects through the endothelial PI3K-AKT-eNOS pathway in rat papillary muscles and isolated cardiomyocytes. Catestatin (rat) maintains mitochondrial membrane potential in I/R cardiomyocytes and increases phosphorylation of AKT at S473, GSK3β at S9, PLB at T17, and eNOS at S1179. Catestatin (rat) reverses desensitization of 22Na + uptake. Catestatin (rat) can be used for the study of nicotinic cholinergic receptor regulation and catecholamine release control mechanisms .
|
-
-
- HY-173005
-
|
|
PI3K
Akt
GSK-3
Apoptosis
|
Cardiovascular Disease
|
|
JZ19 reduces the LDH and ROS levels, and exhibits antioxidant activity against oxygen-glucose deprivation (OGD)-induced cardiomyocyte injury. JZ19 reverses Isoproterenol (HY-B0468)-induced cardiomyocyte hypertrophy and apoptosis through PI3K-AKT-GSK3β signaling pathway. JZ19 alleviates Isoproterenol (HY-B0468)-induced heart failure in mouse models .
|
-
-
- HY-N0815R
-
|
Bufogenin (Standard); Recibufogenin (Standard)
|
Reference Standards
Others
|
Cancer
|
|
Resibufogenin (Standard) is the analytical standard of Resibufogenin. This product is intended for research and analytical applications. Resibufogenin is an orally active anticancer agent. Resibufogenin can be extracted from toad venom. Resibufogenin blocks signaling pathways such as PI3K/Akt, NF-κB, AP-1, activates GSK-3β, and regulates cyclin D1. Resibufogenin can activate central neurons. Resibufogenin has anti-inflammatory activity. Resibufogenin has anti-tumor effects on a variety of tumors such as multiple myeloma, renal cancer, colorectal cancer, pancreatic cancer, and glioma .
|
-
-
- HY-N0695R
-
|
Gomisin-B (Standard); Wuweizi ester-B (Standard); Schisantherin-B (Standard)
|
Reference Standards
PI3K
Akt
mTOR
GSK-3
Tau Protein
TNF Receptor
Interleukin Related
Apoptosis
|
Neurological Disease
Inflammation/Immunology
|
|
Schisantherin B (Gomisin-B) (Standard) is the analytical standard of Schisantherin B. This product is intended for research and analytical applications. Schisantherin B is a lignan compound and one of the active components of Schisandra chinensis. Schisantherin B activates the PI3K/AKT signaling pathway, restores the activity of GSK3β, and reduces the hyperphosphorylation of tau protein in hippocampal and cerebral cortical tissues. Schisantherin B upregulates the level of GLT-1, decreases the expression of pro-inflammatory cytokines TNF-α/IL-1β/IL-6, upregulates the expression of IL-10, and inhibits cell apoptosis. Schisantherin B is applicable to the research of spinal cord injury, Alzheimer's disease and depression.
|
-
-
- HY-B1203S
-
|
9α-Fludrocortisone-d5; 9α-Fluorcortisol-d5
|
Isotope-Labeled Compounds
Mineralocorticoid Receptor
Glucocorticoid Receptor
Apoptosis
|
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
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.
|
-
-
- HY-B1203R
-
|
9α-Fludrocortisone (Standard); 9α-Fluorcortisol (Standard)
|
Reference Standards
Mineralocorticoid Receptor
Glucocorticoid Receptor
Apoptosis
|
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
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.
|
-
-
- HY-B1203S1
-
|
9α-Fludrocortisone-d2; 9α-Fluorcortisol-d2
|
Isotope-Labeled Compounds
Mineralocorticoid Receptor
Glucocorticoid Receptor
Apoptosis
|
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
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.
|
-
-
- HY-158017
-
|
|
PI3K
|
Cancer
|
|
WXM-1-170 (compound 10) is a Indisulam (HY-13650) derivative,and inhibits the migration of gastric cancer cells. WXM-1-170 attenuates PI3K/AKT/GSK-3β/β-catenin signaling pathway .
|
-
-
- HY-161362
-
|
|
PI3K
|
Cancer
|
|
SR-3-65 (compound 6) is a Indisulam (HY-13650) derivative,and inhibits the migration of gastric cancer cells. SR-3-65 attenuates PI3K/AKT/GSK-3β/β-catenin signaling pathway .
|
-
-
- HY-15244G
-
|
|
PI3K
Apoptosis
|
Cancer
|
|
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
|
-
-
- HY-177149
-
|
|
Drug Derivative
|
Neurological Disease
|
|
Allantoin ascorbate is a complexe of Allantoin (HY-N0543). Allantoin is a skin conditioning agent that promotes healthy skin, stimulates new and healthy tissue growth. Allantoin enhances cognitive functions by the mediation of PI3K-Akt-GSK-3β signal pathway. Allantoin ascorbate is slao a skin conditioning agent .
|
-
| Cat. No. |
Product Name |
Type |
-
- HY-15244G
-
|
|
Fluorescent Dyes
|
|
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
|
| Cat. No. |
Product Name |
Type |
-
- HY-15244G
-
|
|
Biochemical Assay Reagents
|
|
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
|
| Cat. No. |
Product Name |
Target |
Research Area |
-
- HY-P6292
-
|
|
PACAP Receptor
PKA
ERK
PI3K
Akt
GSK-3
|
Neurological Disease
Cancer
|
|
KS-133 is a bicyclic peptide with VIPR2 antagonistic activity that can cross the blood-brain barrier. KS-133 selectively blocks VIPR2-mediated Gq/Ca, Gs/cAMP, cAMP/PKA/ERK and PI3K/AKT/GSK3β signaling pathways. KS-133 inhibits VIPR2 agonist-induced CREB phosphorylation in the prefrontal cortex of mice. KS-133 shifts the polarization direction of macrophages toward M1. KS-133 attenuates cancer cell proliferation and reduces the cell cycle distribution level at the S-M phase. KS-133 exerts antitumor effects in a mouse model of colorectal cancer. KS-133 reverses cognitive decline in mouse models of psychiatric disorders. KS-133 can be used for research related to schizophrenia, colorectal cancer and breast cancer .
|
-
- HY-P11313
-
|
Rat chromogranin A367–387
|
nAChR
Akt
|
Cardiovascular Disease
|
|
Catestatin (rat) (Rat chromogranin A367–387) is a potent, reversible, noncompetitive, and noncooperative nicotinic cholinergic antagonist derived from chromogranin A (A367-387). Catestatin (rat) inhibits norepinephrine release in rat PC12 pheochromocytoma cells (IC50 = 1.2 μM), and blocks desensitization of norepinephrine release (IC50 = 0.62 μM). Catestatin (rat) exerts antiadrenergic effects through the endothelial PI3K-AKT-eNOS pathway in rat papillary muscles and isolated cardiomyocytes. Catestatin (rat) maintains mitochondrial membrane potential in I/R cardiomyocytes and increases phosphorylation of AKT at S473, GSK3β at S9, PLB at T17, and eNOS at S1179. Catestatin (rat) reverses desensitization of 22Na + uptake. Catestatin (rat) can be used for the study of nicotinic cholinergic receptor regulation and catecholamine release control mechanisms .
|
| Cat. No. |
Product Name |
Category |
Target |
Chemical Structure |
-
- HY-N0721
-
-
-
- HY-N0815
-
-
-
- HY-125848
-
|
|
Panax ginseng C. A. Meyer
Triterpenes
Structural Classification
Classification of Application Fields
Terpenoids
Plants
Endogenous metabolite
Disease Research Fields
Araliaceae
Source Classification
Cancer
|
Apoptosis
AMPK
PPAR
p38 MAPK
PI3K
Akt
GSK-3
Reactive Oxygen Species (ROS)
SOD
Caspase
|
|
Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota . Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma .
|
-
-
- HY-N0695
-
-
-
- HY-N6064
-
-
-
- HY-N6580
-
-
-
- HY-N7363
-
-
-
- HY-N0721R
-
-
-
- HY-N0815R
-
|
Bufogenin (Standard); Recibufogenin (Standard)
|
Structural Classification
Animals
Steroids
Source Classification
|
Reference Standards
Others
|
|
Resibufogenin (Standard) is the analytical standard of Resibufogenin. This product is intended for research and analytical applications. Resibufogenin is an orally active anticancer agent. Resibufogenin can be extracted from toad venom. Resibufogenin blocks signaling pathways such as PI3K/Akt, NF-κB, AP-1, activates GSK-3β, and regulates cyclin D1. Resibufogenin can activate central neurons. Resibufogenin has anti-inflammatory activity. Resibufogenin has anti-tumor effects on a variety of tumors such as multiple myeloma, renal cancer, colorectal cancer, pancreatic cancer, and glioma .
|
-
-
- HY-N0695R
-
-
| Cat. No. |
Product Name |
Chemical Structure |
-
- HY-B1203S
-
|
|
|
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.
|
-
-
- HY-B1203S1
-
|
|
|
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.
|
-
| Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
-
- HY-15244G
-
|
|
PI3K
Apoptosis
|
Cancer
|
|
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
|
-
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