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Pathways Recommended:	PI3K/Akt/mTOR

Results for "

Akt inhibition

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (21) AMPK (1) Androgen Receptor (1) Apoptosis (23) Autophagy (9) Bcl-2 Family (1) Caspase (2) COX (3) Cytochrome P450 (1) ERK (1) FAK (1) FXR (1) HSP (3) IKK (3) JNK (1) Microtubule/Tubulin (2) MMP (1) mTOR (2) NF-κB (4) Organoid (2) P-glycoprotein (1) p38 MAPK (2) PARP (1) Phosphatase (2) PI3K (9) Polo-like Kinase (PLK) (2) Prolyl Endopeptidase (PREP) (2) PROTACs (1) Ras (1) VEGFR (1)
By Research Areas:	Cancer (33) Infection (1) Inflammation/Immunology (8) Neurological Disease (3)
Click Chemistry:	Alkynes (2)

Inhibitors & Agonists

Screening Libraries

Peptides

Natural
Products

Click Chemistry

Targets Recommended: Akt

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-15186

Ipatasertib Maximum Cited Publications 39 Publications Verification GDC-0068; RG7440	Organoid Akt Apoptosis	Cancer
Ipatasertib (GDC-0068) is an orally active, highly selective and ATP-competitive pan-Akt inhibitor with IC₅₀ values of 5, 18, 8 nM for *Akt1/2/3, respectively. Ipatasertib synchronously activates FoxO3a and NF-κB through inhibition* of *Akt* leading to p53-independent activation of PUMA. Ipatasertib also induces apoptosis in cancer cells and inhibits tumor growth in xenograft mouse models .

HY-N4182

Licochalcone E	Akt p38 MAPK Autophagy	Inflammation/Immunology
Licochalcone E, a flavonoid compound isolated from Glycyrrhiza uralensis, inhibits NF-κB and AP-1 transcriptional activity through the inhibition of *AKT* and MAPK activation .

HY-19934A

Pifusertib hydrochloride TAS-117 hydrochloride	Akt Apoptosis Autophagy	Cancer
Pifusertib (TAS-117) hydrochloride is a potent, selective, orally active allosteric *Akt* inhibitor (with IC₅₀s of 4.8, 1.6, and 44 nM for Akt1, 2, and 3, respectively). Pifusertib hydrochloride triggers anti-myeloma activities and enhances fatal endoplasmic reticulum (ER) stress induced by proteasome inhibition. Pifusertib hydrochloride induces apoptosis and autophagy .

HY-121222

alpha-Bisabolol	PI3K Apoptosis	Cancer
alpha-Bisabolol, an orally active sesquiterpene alcohol, induces cell cycle arrest, mitochondrial apoptosis and inhibition of *PI3K/Akt* signalling pathways. alpha-Bisabolol exerts a protective action against Cisplatin (HY-17394)-induced nephrotoxicity by mitigating inflammation and oxidative stress through the inhibition of NFκB activation. alpha-Bisabolol exhibits anti-inflammatory, analgesic, antibiotic and anticancer activities .

HY-P10049

TAT-TCL1-Akt-in	Akt	Cancer
TAT-TCL1-Akt-in is an Akt inhibitor .

HY-15186C

Ipatasertib tosylate GDC-0068 tosylate; RG7440 tosylate	Organoid Akt Apoptosis	Cancer
Ipatasertib (GDC-0068) tosylate is an orally active, highly selective and ATP-competitive pan-Akt inhibitor with IC₅₀ values of 5, 18, 8 nM for *Akt1/2/3, respectively. Ipatasertib tosylate synchronously activates FoxO3a and NF-κB through inhibition* of *Akt* leading to p53-independent activation of PUMA. Ipatasertib tosylate also induces apoptosis in cancer cells and inhibits tumor growth in xenograft mouse models .

HY-P1115

AKTide-2T	Akt	Others
AKTide-2T is an excellent in vitro substrate for *AKT* and shows competitive inhibition of histone H2B phosphorylation with a K_i of 12 nM. AKTide-2T mimics the optimal phosphorylation sequence of Akt and is an inhibitory peptide with the wildtype AKTide lacking Thr in the S22 position .

HY-P1115A

AKTide-2T TFA	Akt	Others
AKTide-2T TFA is an excellent in vitro substrate for *AKT* and shows competitive inhibition of histone H2B phosphorylation with a K_i of 12 nM. AKTide-2T TFA mimics the optimal phosphorylation sequence of Akt and is an inhibitory peptide with the wildtype AKTide lacking Thr in the S22 position .

HY-19934

Pifusertib TAS-117	Akt Apoptosis Autophagy	Cancer
Pifusertib (TAS-117) is a potent, selective, orally active allosteric *Akt* inhibitor (with IC₅₀s of 4.8, 1.6, and 44 nM for Akt1, 2, and 3, respectively). Pifusertib triggers anti-myeloma activities and enhances fatal endoplasmic reticulum (ER) stress induced by proteasome inhibition. Pifusertib induces apoptosis and autophagy .

HY-163533

CPD-002	VEGFR	Inflammation/Immunology
CPD-002 is an inhibitor for vascular endothelial growth factor receptor 2 (VEGFR 2), that inhibits angiogenesis through inhibition of VEGFR2/PI3K/AKT signaling pathway. CPD-002 exhibits anti-inflammatory activity and attenuates rheumatoid arthritis .

HY-103224

PIT-1	PI3K	Cancer
PIT-1 is a selective PIP3 (phosphatidylinositol 3,4,5-trisphosphate) antagonist. PIT-1 inhibits cancer cell survival and induces apoptosis by inhibition of PIP3 dependent PI3K / Akt signaling. PIT-1 exhibits antitumor activity in vivo .

HY-N0284

Esculetin 4 Publications Verification	PI3K Akt	Inflammation/Immunology Cancer
Esculetin is an active ingredient extracted mainly from the bark of Fraxinus rhynchophylla. Esculetin inhibits platelet-derived growth factor (PDGF)-induced airway smooth muscle cells (ASMCs) phenotype switching through inhibition of *PI3K/Akt* pathway. Esculetin has antioxidant, antiinflammatory, and antitumor activities .

HY-144450

PI3K-IN-29	PI3K Akt	Cancer
PI3K-IN-29 is a potent PI3K inhibitor. PI3K-IN-29 displays good inhibition potencies against U87MG, HeLa and HL60 cells with IC₅₀ values of 0.264, 2.04 and 1.14 µM, respectively. PI3K-IN-29 inhibits *PI3K/Akt* pathway by inhibiting phosphorylation of *Akt* that is catalyzed by PI3K .

HY-12037A

Rigosertib 5 Publications Verification ON-01910	Polo-like Kinase (PLK) PI3K Apoptosis	Cancer
Rigosertib (ON-01910) is a multi-kinase inhibitor and a selective anti-cancer agent, which induces apoptosis by inhibition the PI3 kinase/Akt pathway, promots the phosphorylation of histone H2AX and induces G2/M arrest in cell cycle . Rigosertib is a selective and non-ATP-competitive inhibitor of PLK1 with an IC₅₀ of 9 nM .

HY-N3584

Paris saponin VII 2 Publications Verification Chonglou Saponin VII	Akt p38 MAPK P-glycoprotein Bcl-2 Family Caspase PARP Autophagy Apoptosis	Cancer
Paris saponin VII (Chonglou Saponin VII) is a steroidal saponin isolated from the roots and rhizomes of Trillium tschonoskii. Paris saponin VII-induced apoptosis in K562/ADR cells is associated with *Akt/MAPK* and the inhibition of P-gp. Paris saponin VII attenuates mitochondrial membrane potential, increases the expression of apoptosis-related proteins, such as Bax and cytochrome c, and decreases the protein expression levels of Bcl-2, caspase-9, caspase-3, PARP-1, and p-Akt. Paris saponin VII induces a robust autophagy in K562/ADR cells and provides a biochemical basis in the treatment of leukemia .

HY-12037

Rigosertib sodium 5 Publications Verification ON-01910 sodium	Polo-like Kinase (PLK) PI3K Apoptosis	Cancer
Rigosertib sodium (ON-01910 sodium) is a multi-kinase inhibitor and a selective anti-cancer agent, which induces apoptosis by inhibition the *PI3K/Akt* pathway, promotes the phosphorylation of histone H2AX and induces G2/M arrest in cell cycle . Rigosertib sodium is a selective and non-ATP-competitive inhibitor of PLK1 with an IC₅₀ of 9 nM .

HY-N0284R

Esculetin (Standard)	PI3K Akt	Inflammation/Immunology Cancer
Esculetin (Standard) is the analytical standard of Esculetin. This product is intended for research and analytical applications. Esculetin is an active ingredient extracted mainly from the bark of Fraxinus rhynchophylla. Esculetin inhibits platelet-derived growth factor (PDGF)-induced airway smooth muscle cells (ASMCs) phenotype switching through inhibition of PI3K/Akt pathway. Esculetin has antioxidant, antiinflammatory, and antitumor activities .

HY-N2045

Musk ketone 1 Publications Verification	PI3K Akt Apoptosis Cytochrome P450	Neurological Disease
Musk ketone is a widely used artificial fragrance. Musk ketone is also a cytochrome P450 enzyme inducer. Musk ketone shows mutagenic and comutagenic effects in Hep G2 cells and induces neural stem cell proliferation and differentiation in cerebral ischemia via activation of the *PI3K/Akt* signaling pathway. In the brain, musk ketone is neuroprotective against stroke injury through inhibition of cell apoptosis .

HY-N12124

Monascuspiloin Monascinol	Akt mTOR AMPK Androgen Receptor Apoptosis Autophagy	Cancer
Monascuspiloin (Monascinol) exhibits anti-androgenic activity with an IC₅₀ of 7 μM. Monascuspiloin inhibits viability of PC-3 and LNCaP with IC₅₀ of 45 and 47 μM. Monascuspiloin induces apoptosis in LNCaP through inhibition of *Akt/mTOR* signaling pathway, induces autophagy through activation AMPK signaling pathway and arrest cell cycle at G2/M phase in PC-3. Monascuspiloin exhibits antitumor efficacy in mice .

HY-B0808

Oxaprozin Oxaprozinum; Wy21743	COX NF-κB Akt IKK Apoptosis	Inflammation/Immunology Cancer
Oxaprozin is an orally active and potent COX inhibitor, with IC₅₀ values of 2.2 μM for human platelet COX-1 and and 36 μM for IL-1-stimulated human synovial cell COX-2, respectively. Oxaprozin also inhibits the activation of NF-κB. Oxaprozin induces cell apoptosis. Oxaprozin shows anti-inflammatory activity. Oxaprozin-mediated inhibition of the *Akt/IKK/NF-κB* pathway contributes to its anti-inflammatory properties .

HY-145102

NCT-58	HSP Apoptosis	Cancer
NCT-58 is a potent inhibitor of C-terminal HSP90. NCT-58 does not induce the heat shock response (HSR) due to its targeting of the C-terminal region and elicits anti-tumor activity via the simultaneous downregulation of HER family members as well as inhibition of Akt phosphorylation. NCT-58 kills Trastuzumab-resistant breast cancer stem-like cells. NCT-58 induces apoptosis in HER2-positive breast cancer cells .

HY-B0808A

Oxaprozin potassium Oxaprozinum potassium; Wy21743 potassium	COX NF-κB Akt IKK Apoptosis	Inflammation/Immunology Cancer
Oxaprozin potassium is an orally active and potent COX inhibitor, with IC₅₀ values of 2.2 μM for human platelet COX-1 and and 36 μM for IL-1-stimulated human synovial cell COX-2, respectively. Oxaprozin potassium also inhibits the activation of NF-κB. Oxaprozin potassium induces cell apoptosis. Oxaprozin potassium shows anti-inflammatory activity. Oxaprozin potassium-mediated inhibition of the *Akt/IKK/NF-κB* pathway contributes to its anti-inflammatory properties .

HY-15113A

Y-29794 tosylate	Prolyl Endopeptidase (PREP)	Neurological Disease Cancer
Y-29794 tosylate is a selective, orally active inhibitor for non-peptide prolyl endopeptidase (PREP), with an IC₅₀ of 3 nM and a K_i of 0.95 nM. Y-29794 tosylate enhances the effect of thyrotropin-releasing hormone (TRH) on the release of ACh in the rat hippocampus, exhibits potential neuroprotective efficacy. Y-29794 tosylate exhibits anticancer activity through inhibition of the *IRS1-AKT-mTORC1* pathway. Y-29794 tosylate penetrates the brain-blood barrier (BBB) .

HY-15113

Y-29794	Prolyl Endopeptidase (PREP)	Neurological Disease Cancer
Y-29794 is a selective, orally active inhibitor for non-peptide prolyl endopeptidase (PREP), with an IC₅₀ of 3 nM and a K_i of 0.95 nM. Y-29794 enhances the effect of thyrotropin-releasing hormone (TRH) on the release of ACh in the rat hippocampus, exhibits potential neuroprotective efficacy. Y-29794 exhibits anticancer activity through inhibition of the *IRS1-AKT-mTORC1* pathway. Y-29794 penetrates the brain-blood barrier (BBB) .

HY-156002

LUNA18	Ras ERK	Cancer
LUNA18 is an orally-available cyclic peptide KRAS and ERK inhibitor. LUNA18 phosphorylates ERK and *AKT* and decreases cell proliferation in RAS-mutated cancer cells. LUNA18 exhibits RAS signal inhibition and potent anti-cancer activities through inhibiting interaction between RAS and guanine nucleotide exchange factors (GEFs) in a mouse xenograft model. LUNA18 shows significant cellular efficacy against cell lines with KRAS genetic alterations, such as colon cancer, stomach cancer, non-small cell lung cancer and pancreaticcancer .

HY-B0808R

Oxaprozin (Standard) Oxaprozinum (Standard); Wy21743 (Standard)	COX NF-κB Akt IKK Apoptosis	Inflammation/Immunology Cancer
Oxaprozin (Standard) is the analytical standard of Oxaprozin. This product is intended for research and analytical applications. Oxaprozin is an orally active and potent COX inhibitor, with IC₅₀ values of 2.2 μM for human platelet COX-1 and and 36 μM for IL-1-stimulated human synovial cell COX-2, respectively. Oxaprozin also inhibits the activation of NF-κB. Oxaprozin induces cell apoptosis. Oxaprozin shows anti-inflammatory activity. Oxaprozin-mediated inhibition of the *Akt/IKK/NF-κB* pathway contributes to its anti-inflammatory properties .

HY-13270

ABT-751 E7010	Microtubule/Tubulin Autophagy Apoptosis	Cancer
ABT-751 (E7010) is a novel, highly orally bioavailable sulfonamides antimitotic compound and tubulin binder. It prevents tubulin aggregation by binding to the colchicine site on β-tubulin, leading to cell cycle arrest in G2/M phase and inducing apoptosis, thus effectively preventing cell division. ABT-751 induces autophagy by inhibiting the AKT/MTOR signaling pathway. ABT-751 showed significant inhibition against various types of cancer cells, including lung, gastric, colon, and breast cancer .

HY-132231

FD223	PI3K Apoptosis	Cancer
FD223 is a potent and selective phosphoinositide 3-kinase delta (PI3Kδ) inhibitor. FD223 displays high potency (IC₅₀=1 nM) and good selectivity over other isoforms (IC₅₀s of 51 nM, 29 nM and 37 nM, respectively for α, β and γ). FD223 exhibits efficient inhibition of the proliferation of acute myeloid leukemia (AML) cell lines by suppressing p-AKT Ser473 thus causing G1 phase arrest during the cell cycle. FD223 has potential for the research of leukemia such as AML .

HY-146325

HSP90-IN-11	HSP	Cancer
HSP90-IN-11 (Compound 12c) is a potent inhibitor of HSP90. HSP90-IN-11 displays potent HSP90α inhibition comparable to AUY-922 (Luminespib). HSP90-IN-11 shows significant antiproliferative activity in CRC and NSCLC cells in a double digit nM range. HSP90-IN-11 leads to rapid degradation of client proteins EGFR and Akt in NSCLC cells. HSP90-IN-11 induces significant accumulation of a sub-G1 phase population .

HY-107738

Guggulsterone 10+ Cited Publications Z/E-Guggulsterone	Apoptosis JNK Akt Caspase FXR Autophagy	Cancer
Guggulsterone is a plant sterol derived from the gum resin of the tree Commiphora wightii. Guggulsterone inhibits the growth of a wide variety of tumor cells and induces apoptosis through down regulation of antiapoptotic gene products (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP and survivin), modulation of cell cycle proteins (cyclin D1 and c-Myc), activation of caspases and JNK, inhibition of *Akt* . Guggulsterone, a farnesoid X receptor (FXR) antagonist, decreases CDCA-induced FXR activation with IC₅₀s of 17 and 15 μM for Z- and E-Guggulsterone, respectively .

HY-13270A

ABT-751 hydrochloride E7010 hydrochloride	Microtubule/Tubulin Autophagy Apoptosis	Cancer
ABT-751 (E7010) hydrochloride is a novel, highly orally bioavailable sulfonamides antimitotic compound and tubulin binder. It prevents tubulin aggregation by binding to the colchicine site on β-tubulin, leading to cell cycle arrest in G2/M phase and inducing apoptosis, thus effectively preventing cell division. ABT-751 (E7010) hydrochloride induces autophagy by inhibiting the AKT/MTOR signaling pathway. ABT-751 (E7010) hydrochloride showed significant inhibition against various types of cancer cells, including lung, gastric, colon, and breast cancer .

HY-19542

C6 Ceramide 2 Publications Verification C6-Cer; N-Hexanoylsphingosine	Apoptosis	Cancer
C6 Ceramide (C6-Cer) is a short-chain, cell-permeable ceramide pathway activator with anticancer activity. C6 Ceramide-mediated miR-29b expression participates in the progression of multiple myeloma through suppressing the proliferation, migration and angiogenesis of endothelial cells by targeting Akt signal pathway. C6 Ceramide exhibits multiple anti-cancer properties including cell cycle arrest, Apoptosis, inhibition of tumor growth and enhances the effects of chemotherapy in drug-resistant cancer cells. C6-ceramide can be used as an adjuvant for chemotherapeutic agents, to enhance anti-tumor effects .

HY-151137

HSP90/mTOR-IN-1	mTOR HSP Apoptosis Autophagy	Cancer
HSP90/mTOR-IN-1 is a potent and orally active Hsp90 and mTOR inhibitor with IC₅₀ values of 69 nM and 29 nM, respectively. HSP90/mTOR-IN-1 suppresses the proliferation of SW780 cells through the over-activation of the *PI3K/AKT/mTOR* pathway. HSP90/mTOR-IN-1 induces apoptosis and autophagy via selective Hsp90 and mTOR inhibition. HSP90/mTOR-IN-1 also has considerable in vivo anti-tumor activity. HSP90/mTOR-IN-1 can be used for researching bladder cancer .

HY-N3387

Licoricidin	Apoptosis NF-κB Akt MMP	Inflammation/Immunology Cancer
Licoricidin (LCD) is isolated from Glycyrrhiza uralensis Fisch, possesses anti-cancer activities. Licoricidin (LCD) inhibit SW480 cells (IC₅₀=7.2 μM) by inducing cycle arrest, apoptosis and autophagy, and is a potential chemopreventive or chemotherapeutic agent against colorectal cancer . Licoricidin (LCD) inhibits Lung Metastasis by inhibition of tumor angiogenesis and lymphangiogenesis as well as changes in the local microenvironment of tumor tissues the anticarcinogenic effect . Licoricidin enhanced gemcitabine-induced cytotoxicity in Osteosarcoma (OS) cells by inactivation of the *Akt* and NF-κB pathways in vitro and in vivo . Licoricidin blocks UVA-induced photoaging via ROS scavenging, limits the activity of MMP-1, it can be considered as an active ingredient in new topically applied anti-ageing formulations .

HY-135699

TD52 1 Publications Verification	Apoptosis Phosphatase Akt	Cancer
TD52, an Erlotinib (HY-50896) derivative, is an orally active, potent cancerous inhibitor of protein phosphatase 2A (CIP2A) inhibitor. TD52 mediates the apoptotic effect in triple-negative breast cancer (TNBC) cells via regulating the CIP2A/PP2A/p-Akt signalling pathway. TD52 indirectly reduced CIP2A by disturbing Elk1 binding to the CIP2A promoter. TD52 has less p-EGFR inhibition and has potent anti-cancer activity . TD52 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

HY-135699A

TD52 dihydrochloride 1 Publications Verification	Akt Phosphatase Apoptosis	Cancer
TD52 dihydrochloride, an Erlotinib (HY-50896) derivative, is an orally active, potent cancerous inhibitor of protein phosphatase 2A (CIP2A) inhibitor. TD52 dihydrochloride mediates the apoptotic effect in triple-negative breast cancer (TNBC) cells via regulating the CIP2A/PP2A/p-Akt signalling pathway. TD52 dihydrochloride indirectly reduced CIP2A by disturbing Elk1 binding to the CIP2A promoter. TD52 dihydrochloride has less p-EGFR inhibition and has potent anti-cancer activity . TD52 (dihydrochloride) is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

HY-116497

PH11	Others	Cancer
PH11 is a novel focal adhesion kinase (FAK) inhibitor that rapidly induces apoptosis in TRAIL-resistant PANC-1 cells when combined with TRAIL, but has no effect on normal human fibroblasts. The study found that PH11 downregulates c-FLIP through inhibition of FAK and phosphatidylinositol-3-kinase (PI3K)/AKT pathways, thereby restoring the TRAIL apoptotic pathway, suggesting that this combination therapy may provide an attractive therapeutic strategy for the safe and effective treatment of pancreatic cancer. PH11 selectively inhibits c-FLIP expression by modulating upstream signaling pathways and may represent an innovative therapeutic strategy. Although further work is needed to fully elucidate the mechanism of PH11-induced TRAIL sensitization, we believe that our results will provide a new approach to target c-FLIP without the risk of interfering with caspase-8 processing, which could potentially lead to TRAIL resistance. This study also suggests a role for the FAK/AKT signaling pathway in regulating c-FLIP expression in TRAIL-induced apoptosis, and this understanding will provide important clues to control the resistance mechanism to optimize the potential of TRAIL-based pancreatic cancer treatment.

HY-W130965

1-Formyl-beta-carboline	Others	Infection
1-Formyl-beta-carboline is an alkaloid with inhibitory activity against Newcastle disease virus (NDV). 1-Formyl-beta-carboline can effectively inhibit different genotypes of NDV with IC50 values within 10 μM, and its inhibition rate is more than 90% at a concentration of 20 μM. 1-Formyl-beta-carboline mainly exerts its effects by inhibiting the adsorption and entry processes in the NDV life cycle. 1-Formyl-beta-carboline has been identified as a novel HN inhibitor that can directly interact with the NDV HN protein and affect the adsorption of NDV. 1-Formyl-beta-carboline also inhibits the entry of NDV by inhibiting the PI3K/Akt signaling pathway rather than the ERK pathway .

HY-163709

PROTAC FAK degrader 2	PROTACs FAK	Cancer
PROTAC FAK degrader 2 (Compound F2) is a PROTAC degrader for focal adhesion kinase (FAK), with DC₅₀ of 27.72 and 60.1 nM, for total FAK and phosphorylated p-FAK. PROTAC FAK degrader 2 inhibits cell viability of cancer cells 4T1, MDA-MB-231, MDA-MB-468 and MDA-MB-435, with IC₅₀s of 0.73-5.84 μM. PROTAC FAK degrader 2 reverses the multidrug resistance (MDR) through inhibition of *AKT* and ERK signaling pathway. PROTAC FAK degrader 2 exhibits antitumor efficacy in HCT/8 xenograft mouse model. (Pink: ligand for target protein Ifebemtinib (HY-122844); Black: linker (HY-Y0681); Blue: ligand for E3 ligase Thalidomide (HY-14658))

Cat. No.	Product Name

HY-L015

PI3K/Akt/mTOR Compound Library	600 compounds
The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials. MCE owns a unique collection of 600 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

PI3K/Akt/mTOR Compound Library

600 compounds

The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials.

MCE owns a unique collection of 600 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

Cat. No.	Product Name	Target	Research Area