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Pathways Recommended:	Neuronal Signaling JAK/STAT Signaling

Results for "

oncogenic signaling

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (1) Apoptosis (8) c-Met/HGFR (2) c-Myc (1) CDK (1) DYRK (1) Endogenous Metabolite (1) Farnesyl Transferase (3) Glutaminase (2) Hedgehog (2) HSP (2) iGluR (2) MEK (2) PAK (3) PKC (2) PROTACs (1) PTEN (1) Raf (1) Ras (4) RET (2) Smo (1) TGF-beta/Smad (1) Tyrosinase (2) Wnt (1)
By Research Areas:	Cancer (22) Infection (3) Inflammation/Immunology (2) Metabolic Disease (2) Neurological Disease (2)

Inhibitors & Agonists

Screening Libraries

Peptides

Natural
Products

Targets Recommended: RGS Protein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-106381A

Aurothiomalate tetramer sodium	PKC	Inflammation/Immunology
Aurothiomalate tetramer sodium, an Aurothiomalate sodium (HY-106381) tetrameric form, is antiarthritic gold agent. Aurothiomalate sodium is a potent and selective oncogenic PKCι signaling inhibitor .

HY-108508

SMANT hydrochloride	Smo Hedgehog	Cancer
SMANT hydrochloride is a Smoothened (Smo) signaling inhibitor. SMANT hydrochloride is antagonist of Smo accumulation within the primary cilium (PC). SMANT hydrochloride has an equivalent activity in inhibiting SmoM2 (oncogenic form of Smo) and wild-type Smo .

HY-15872A

FTI-277 hydrochloride 5 Publications Verification	Farnesyl Transferase Apoptosis Ras	Infection Cancer
FTI-277 hydrochloride is an inhibitor of farnesyl transferase (FTase); a highly potent Ras CAAX peptidomimetic which antagonizes both H- and K-Ras oncogenic signaling. FTI-277 hydrochloride can inhibit hepatitis delta virus (HDV) infection.

HY-13007

PF-3758309 Maximum Cited Publications 9 Publications Verification PF-03758309	PAK Apoptosis	Cancer
PF-3758309 (PF-03758309) is a potent, orally available, and reversible ATP-competitive inhibitor of PAK4 (K_d= 2.7 nM; K_i=18.7 nM). PF-3758309 has the expected cellular functions of a PAK4 inhibitor: inhibition of anchorage-independent growth, induction of apoptosis, cytoskeletal remodeling, and inhibition of proliferation .

HY-150926

G12Si-1	Ras	Cancer
G12Si-1 is a selective K-Ras(G12S) covalent inhibitor, which can inhibit oncogenic signaling of K-Ras(G12S). G12Si-1 shows good ability to covalently engage recombinant K-Ras(G12S) at the mutant serine residue. G12Si-1 can also affect nucleotide cycling of K-Ras by blocking Sos-catalyzed exchange and decreasing the rate of EDTA promoted exchange .

HY-164482

HG-6-63-01	RET	Cancer
HG-6-63-01 is a type II RET tyrosine kinase inhibitor (TKI). HG-6-63-01 also inhibits REarranged during Transfection (RET) kinase and signaling in human thyroid cancer cell lines carrying oncogenic RET alleles. HG-6-63-01 impairs phosphorylation and signalling of RET oncogenic mutants. HG-6-63-01 blunts proliferation of RET/C634R and RET/M918T-transformed fibroblasts and of RET mutant thyroid cancer cells, which is promising for research of cancers harboring oncogenic activation of RET .

HY-P10488

cycFWRPW	Wnt Others	Cancer
cycFWRPW is a peptide inhibitor of TLE1. TLE1 is an oncogenic transcriptional co‐repressor that exerts its repressive effects through binding of transcription factors, and inhibits Wnt signaling .

HY-15872

FTI-277	Farnesyl Transferase Apoptosis Ras	Infection Cancer
FTI-277 is an inhibitor of farnesyl transferase (FTase); a highly potent Ras CAAX peptidomimetic which antagonizes both H- and K-Ras oncogenic signaling. FTI-277 can inhibit hepatitis delta virus (HDV) infection.

HY-N11794

7-Ketologanin	Others	Others
7-Ketologanin is an iridoid glucoside. 7-Ketologanin can be isolated from the Stems of Viburnum erosum. 7-Ketologanin involves in biosynthetic pathway of oleuropein. Oleuropein, is a bioactive phenolic compound, modulates several oncogenic signalling pathways .

HY-13007A

PF-3758309 hydrochloride PF-03758309 hydrochloride	PAK Apoptosis	Cancer
PF-3758309 (PF-03758309) hydrochloride is a potent, orally available, and reversible ATP-competitive inhibitor of PAK4 (K_d= 2.7 nM; K_i=18.7 nM). PF-3758309 hydrochloride has the expected cellular functions of a PAK4 inhibitor: inhibition of anchorage-independent growth, induction of apoptosis, cytoskeletal remodeling, and inhibition of proliferation .

HY-13007B

PF-3758309 dihydrochloride PF-03758309 dihydrochloride	PAK Apoptosis	Cancer
PF-3758309 (PF-03758309) dihydrochloride is a potent, orally available, and reversible ATP-competitive inhibitor of PAK4 (K_d= 2.7 nM; K_i=18.7 nM). PF-3758309 dihydrochloride has the expected cellular functions of a PAK4 inhibitor: inhibition of anchorage-independent growth, induction of apoptosis, cytoskeletal remodeling, and inhibition of proliferation .

HY-106381

Aurothiomalate sodium	PKC	Inflammation/Immunology Cancer
Aurothiomalate sodium is a potent and selective oncogenic PKC_ι signaling inhibitor. Aurothiomalate sodium inhibits tumor cell proliferation and not cell apoptosis. Aurothiomalate sodium is a potent thioredoxin reductase (TrxR) inhibitor. Aurothiomalate sodium, an anti-rheumatoid agent, exhibits potent anti-tumor activity .

HY-164548

WK88-1	HSP Apoptosis	Cancer
WK88-1, a Hsp90 inhibitor, induces overall degradation of multiple oncogenic signaling molecules including EGFR, ErbB2 and ErbB3, leading to subsequent growth arrest and apoptosis in the Gefitinib-resistant H1975 cell line .

HY-110038

FTI-277 TFA	Farnesyl Transferase Apoptosis Ras	Infection Cancer
FTI-277 TFA is an inhibitor of farnesyl transferase (FTase); a highly potent Ras CAAX peptidomimetic which antagonizes both H- and K-Ras oncogenic signaling. FTI-277 TFA can inhibit hepatitis delta virus (HDV) infection.

HY-119607

DYRKi	DYRK	Cancer
DYRKi is an inhibitor of DYRK1 and DYRK1B with IC₅₀ values of 3.7 µM and 90 nM, respectively, which is used as a potent antagonist of Hh/Gli signaling. DYRKi impairs SMO-dependent and SMO-independent oncogenic GLI activity in human medulloblastoma cells. DYRKi is promising for research of HH/GLI-associated cancers .

HY-100627A

APS-2-79 hydrochloride	MEK	Cancer
APS-2-79 hydrochloride is a KSR-dependent MEK antagonist. APS-2-79 inhibits ATP ^biotin binding to KSR2 within the KSR2-MEK1 complexe with an IC₅₀ of 120 nM. APS-2-79 makes the stabilization of the KSR inactive state antagonizes oncogenic Ras-MAPK signaling .

HY-100627

APS-2-79	MEK	Cancer
APS-2-79 is a KSR-dependent MEK antagonist. APS-2-79 inhibits ATP ^biotin binding to KSR2 within the KSR2-MEK1 complexe with an IC₅₀ of 120 nM. APS-2-79 makes the stabilization of the KSR inactive state antagonizes oncogenic Ras-MAPK signaling .

HY-170791

CIB-L43	PTEN TGF-beta/Smad Akt	Cancer
CIB-L43 is an orally active TRBP inhibitor (K_D = 4.78 nM) and enhances disruption of TRBP-Dicer interactions (IC₅₀ = 2.34 μM). CIB-L43 suppresses oncogenic miR-21 biosynthesis, increasing PTEN and Smad7 expression and inhibiting AKT and TGF-β signaling, thereby reducing HCC cell proliferation and migration .

HY-156084

LL-K9-3	CDK PROTACs Apoptosis c-Myc	Cancer
LL-K9-3 is a potent small-molecule degrader of CDK9-cyclin T1. LL-K9-3 has anti-proliferative and pro-apoptotic activities and suppresses downstream signaling of CDK9 and AR. Moreover, LL-K9-3 inhibits AR and Myc-driven oncogenic transcriptional programs .

HY-P10436

Braftide	Raf	Cancer
Braftide is an allosteric inhibitor for BRAF kinase by targeting the dimer interface of BRAF kinase and inhibiting the formation of BRAF dimers. Braftide inhibits wild-type BRAF and oncogenic BRAF ^G469A with IC₅₀ of 364 nM and 172 nM, respectively. Braftide inhibits MAPK signaling pathway, inhibits proliferation of KRAS mutant tumor cells (EC₅₀ is 7.1 and 6.6 μM, for HCT116 and HCT-15), in combination of TAT sequence .

HY-143400

HSP70-IN-3	HSP Hedgehog	Cancer
HSP70-IN-3 is a potent HSP70 inhibitor (IC₅₀s of 1.1 and 1.9 μM in ASZ001 and C3H10T1/2, respectively). HSP70-IN-3 has anti-Hh (Hedgehog signaling) activity and anti-proliferative activity and reduces expression of the oncogenic transcription factor GLI1 .

HY-W015309

Decanoic acid 2 Publications Verification	iGluR Tyrosinase c-Met/HGFR Glutaminase Endogenous Metabolite	Neurological Disease Metabolic Disease Cancer
Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

HY-164549

XMD15-44	RET	Cancer
XMD15-44 is a RET kinase inhibitor.XMD15-44 has a growth-inhibitory effect on RET/C634R and RET/M918T transformed RAT1 cells, with IC₅₀ values of 11.5 nM and 8.3 nM, respectively. XMD15-44 can inhibit RET kinase and signaling in human thyroid cancer cell lines carrying oncogenic RET alleles, reducing cell proliferation .

HY-W015309R

Decanoic acid (Standard)	iGluR Tyrosinase c-Met/HGFR Glutaminase	Neurological Disease Metabolic Disease Cancer
Decanoic acid (Standard) is the analytical standard of Decanoic acid. This product is intended for research and analytical applications. Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

Cat. No.	Product Name

HY-L064

Glutamine Metabolism Compound Library	1,151 compounds
Glutamine is an important metabolic fuel that helps rapidly proliferating cells meet the increased demand for ATP, biosynthetic precursors, and reducing agents. Glutamine Metabolism pathway involves the initial deamination of glutamine by glutaminase(GLS), yielding glutamate and ammonia. Glutamate is converted to the TCA cycle intermediate α-ketoglutarate (α-KG) by either glutamate dehydrogenase (GDH) or by the alanine or aspartate transaminases (TAs), to produce both ATP and anabolic carbons for the synthesis of amino acids, nucleotides and lipids. During periods of hypoxia or mitochondrial dysfunction, α-KG can be converted to citrate in a reductive carboxylation reaction catalyzed by IDH2. The newly formed citrate exits the mitochondria where it is used to synthesize fatty acids and amino acids and produce the reducing agent, NADPH. Cancer cells display an altered metabolic circuitry that is directly regulated by oncogenic mutations and loss of tumor suppressors. Mounting evidence indicates that altered glutamine metabolism in cancer cells has critical roles in supporting macromolecule biosynthesis, regulating signaling pathways, and maintaining redox homeostasis, all of which contribute to cancer cell proliferation and survival. Thus, intervention in glutamine metabolic processes could provide novel approaches to improve cancer treatment. MCE owns a unique collection of 1,151 compounds targeting the mainly proteins and enzymes involved in glutamine metabolism pathway. Glutamine Metabolism compound library is a useful tool for intervention in glutamine metabolic processes.

Glutamine Metabolism Compound Library

1,151 compounds

Glutamine is an important metabolic fuel that helps rapidly proliferating cells meet the increased demand for ATP, biosynthetic precursors, and reducing agents. Glutamine Metabolism pathway involves the initial deamination of glutamine by glutaminase(GLS), yielding glutamate and ammonia. Glutamate is converted to the TCA cycle intermediate α-ketoglutarate (α-KG) by either glutamate dehydrogenase (GDH) or by the alanine or aspartate transaminases (TAs), to produce both ATP and anabolic carbons for the synthesis of amino acids, nucleotides and lipids. During periods of hypoxia or mitochondrial dysfunction, α-KG can be converted to citrate in a reductive carboxylation reaction catalyzed by IDH2. The newly formed citrate exits the mitochondria where it is used to synthesize fatty acids and amino acids and produce the reducing agent, NADPH.

Cancer cells display an altered metabolic circuitry that is directly regulated by oncogenic mutations and loss of tumor suppressors. Mounting evidence indicates that altered glutamine metabolism in cancer cells has critical roles in supporting macromolecule biosynthesis, regulating signaling pathways, and maintaining redox homeostasis, all of which contribute to cancer cell proliferation and survival. Thus, intervention in glutamine metabolic processes could provide novel approaches to improve cancer treatment.

MCE owns a unique collection of 1,151 compounds targeting the mainly proteins and enzymes involved in glutamine metabolism pathway. Glutamine Metabolism compound library is a useful tool for intervention in glutamine metabolic processes.

Cat. No.	Product Name	Target	Research Area

HY-P10436

Braftide	Raf	Cancer
Braftide is an allosteric inhibitor for BRAF kinase by targeting the dimer interface of BRAF kinase and inhibiting the formation of BRAF dimers. Braftide inhibits wild-type BRAF and oncogenic BRAF ^G469A with IC₅₀ of 364 nM and 172 nM, respectively. Braftide inhibits MAPK signaling pathway, inhibits proliferation of KRAS mutant tumor cells (EC₅₀ is 7.1 and 6.6 μM, for HCT116 and HCT-15), in combination of TAT sequence .

HY-P10488

cycFWRPW	Wnt Peptides	Cancer
cycFWRPW is a peptide inhibitor of TLE1. TLE1 is an oncogenic transcriptional co‐repressor that exerts its repressive effects through binding of transcription factors, and inhibits Wnt signaling .

Decanoic acid 2 Publications Verification	Structural Classification Microorganisms Neurological Disease Classification of Application Fields Ketones, Aldehydes, Acids Source classification Endogenous metabolite Disease Research Fields Biological Pesticide Research Agricultural Research	iGluR Tyrosinase c-Met/HGFR Glutaminase Endogenous Metabolite
Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

7-Ketologanin	Structural Classification Iridoids Terpenoids Source classification Viburnum erosum Thunb. Plants Adoxaceae	Others
7-Ketologanin is an iridoid glucoside. 7-Ketologanin can be isolated from the Stems of Viburnum erosum. 7-Ketologanin involves in biosynthetic pathway of oleuropein. Oleuropein, is a bioactive phenolic compound, modulates several oncogenic signalling pathways .

Decanoic acid (Standard)	Structural Classification Microorganisms Ketones, Aldehydes, Acids Source classification Endogenous metabolite	iGluR Tyrosinase c-Met/HGFR Glutaminase
Decanoic acid (Standard) is the analytical standard of Decanoic acid. This product is intended for research and analytical applications. Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

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