Akt/GSK3β/mTOR signaling pathway

Pathways Recommended:	PI3K/Akt/mTOR MAPK/ERK Pathway Neuronal Signaling JAK/STAT Signaling

By Targets:	Akt (6) GSK-3 (3) mTOR (3) AMPK (2) Apoptosis (9) Autophagy (1) Bcl-2 Family (3) Casein Kinase (2) NF-κB (2) Organoid (1) PI3K (3) Reference Standards (2) TGF-beta/Smad (2)
By Research Areas:	Cancer (9) Cardiovascular Disease (4) Inflammation/Immunology (6) Metabolic Disease (4) Neurological Disease (2)

Targets Recommended: mTOR Tissue Factor Pathway Inhibitor (TFPI) Akt RGS Protein GSK-3

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-10358

MK-2206 dihydrochloride Maximum Cited Publications 462 Publications Verification MK-2206 (2HCl)	Bcl-2 Family Apoptosis mTOR Akt GSK-3	Cardiovascular Disease Inflammation/Immunology Cancer
MK-2206 dihydrochloride (MK-2206 2HCl) is an orally active pan-AKT inhibitor, with IC₅₀ values of 8 nM, 12 nM and 65 nM against **AKT1, AKT2 and AKT3, respectively. MK-2206 dihydrochloride inhibits the Akt/mTOR** signaling pathway and reduces the levels of downstream *GSK3β* and Mcl-1 via proteasomal degradation. MK-2206 dihydrochloride induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 dihydrochloride causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 dihydrochloride can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .

HY-15244

Alpelisib 120+ Cited Publications 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-108232

MK-2206 Maximum Cited Publications 462 Publications Verification	Bcl-2 Family Apoptosis mTOR Akt GSK-3	Metabolic Disease Inflammation/Immunology Cancer
MK-2206 is an orally active pan-AKT inhibitor, with IC₅₀ values of 8 nM, 12 nM and 65 nM against **AKT1, AKT2 and AKT3, respectively. MK-2206 inhibits the Akt/mTOR** signaling pathway and reduces the levels of downstream *GSK3β* and Mcl-1 via proteasomal degradation. MK-2206 induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .

HY-N0559

Kirenol 1 Publications Verification	Casein Kinase Apoptosis AMPK Akt NF-κB TGF-beta/Smad	Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a K_d value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the *CK2/AKT* and *AMPK-mTOR-ULK1* pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the *GSK3β, BMP* and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis .

HY-15244A

Alpelisib hydrochloride 120+ Cited Publications 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-10357

MK-2206 free base	Akt mTOR Apoptosis GSK-3 Bcl-2 Family	Metabolic Disease Inflammation/Immunology Cancer
MK-2206 free base is an orally active pan-AKT inhibitor, with IC₅₀ values of 8 nM, 12 nM and 65 nM against **AKT1, AKT2 and AKT3, respectively. MK-2206 free base inhibits the Akt/mTOR** signaling pathway and reduces the levels of downstream *GSK3β* and Mcl-1 via proteasomal degradation. MK-2206 free base induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 free base causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 free base can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .

HY-N0559R

Kirenol (Standard)	Reference Standards Casein Kinase Apoptosis AMPK Akt NF-κB TGF-beta/Smad	Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Kirenol (Standard) is the analytical standard of Kirenol (HY-N0559). This product is intended for research and analytical applications. Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a K_d value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.

HY-10358R

MK-2206 dihydrochloride (Standard) MK-2206 (2HCl) (Standard)	Organoid Reference Standards Akt Autophagy Apoptosis	Cardiovascular Disease Inflammation/Immunology Cancer
MK-2206 dihydrochloride (MK-2206 2HCl) (Standard) is the analytical standard of MK-2206 dihydrochloride (HY-10358). This product is intended for research and analytical applications. MK-2206 dihydrochloride is an orally active pan-AKT inhibitor, with IC₅₀ values of 8 nM, 12 nM and 65 nM against **AKT1, AKT2 and AKT3, respectively. MK-2206 dihydrochloride inhibits the Akt/mTOR** signaling pathway and reduces the levels of downstream *GSK3β* and Mcl-1 via proteasomal degradation. MK-2206 dihydrochloride induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 dihydrochloride causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 dihydrochloride can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .

HY-15244G

Alpelisib	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 .

Cat. No.	Product Name	Type

HY-15244G

Alpelisib	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 .

Alpelisib

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

Alpelisib	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 .

Alpelisib

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	Category	Target	Chemical Structure

HY-N0559

Kirenol 1 Publications Verification	Structural Classification Terpenoids Bituminaria morisiana (Pignatti & Metlesics) Greuter Diterpenoids Plants Compositae Source Classification	Casein Kinase Apoptosis AMPK Akt NF-κB TGF-beta/Smad
Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a K_d value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the *CK2/AKT* and *AMPK-mTOR-ULK1* pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the *GSK3β, BMP* and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis .

HY-N0559R

Kirenol (Standard)	Structural Classification Terpenoids Bituminaria morisiana (Pignatti & Metlesics) Greuter Diterpenoids Plants Compositae Source Classification	Reference Standards Casein Kinase Apoptosis AMPK Akt NF-κB TGF-beta/Smad
Kirenol (Standard) is the analytical standard of Kirenol (HY-N0559). This product is intended for research and analytical applications. Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a K_d value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.

Targets Recommended: mTOR Tissue Factor Pathway Inhibitor (TFPI) Akt RGS Protein GSK-3

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-15244G

Alpelisib	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 .

MCE Japan Authorized Agent ナミキ商事株式会社コスモ・バイオ株式会社重松貿易株式会社
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Akt/GSK3β/mTOR signaling pathway

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Fluorescent Dyes

Biochemical Assay Reagents

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GMP Molecules

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