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Pathways Recommended:	Protein Tyrosine Kinase/RTK

Results for "

RTK

" in MedChemExpress (MCE) Product Catalog:

By Targets:	AMPK (1) Apoptosis (8) Autophagy (1) c-Fms (3) c-Kit (10) c-Met/HGFR (5) CDK (1) Discoidin Domain Receptor (2) EGFR (2) FGFR (2) FLT3 (6) HIV (1) Isotope-Labeled Compounds (1) PDGFR (11) Phosphatase (2) SHP2 (4) TAM Receptor (4) Trk Receptor (4) VEGFR (13)
By Research Areas:	Cancer (27) Cardiovascular Disease (1) Infection (1) Inflammation/Immunology (3)

Inhibitors & Agonists

Screening Libraries

Recombinant Proteins

Isotope-Labeled Compounds

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-137092

IACS-13909 1 Publications Verification	SHP2 Phosphatase	Cancer
IACS-13909 is a selective, potent and orally active SHP2 allosteric inhibitor with an IC₅₀ of 15.7 nM and a K_d of 32 nM. IACS-13909 is more selective for SHP2 than other phosphatases (including SHP1). IACS-13909 has antitumor activities and suppresses MAPK pathway signaling in receptor tyrosine kinases (RTK)-dependent cancers .

HY-50905

Dovitinib Maximum Cited Publications 7 Publications Verification CHIR-258; TKI258	FLT3 c-Kit FGFR VEGFR PDGFR c-Fms	Cancer
Dovitinib (CHIR-258) is an orally active, potent multi-targeted tyrosine kinase (RTK) inhibitor with IC₅₀s of 1, 2, 36, 8/9, 10/13/8, 27/210 nM for FLT3, c-Kit, CSF-1R, FGFR1/FGFR3, VEGFR1/VEGFR2/VEGFR3 and PDGFRα/PDGFRβ, respectively. Dovitinib has potent antitumor activity .

HY-148316

hVEGF-IN-2	VEGFR	Cancer
hVEGF-IN-2 (compound 19) is a selective VEGF (Flk-1) receptor tyrosine kinases (RTK) inhibitor with an IC₅₀ value of 2.5 μM. hVEGF-IN-2 inhibits PDGF RTK activity with an IC₅₀ value of 33.1 μM. hVEGF-IN-2 can be used for the development of RTK-specific agents .

HY-144424

Trk-IN-11	Trk Receptor	Cancer
Trk-IN-11 (Compound 14h) is a potent inhibitor of TRK (IC₅₀ = 1.4, 1.8 nM, against TrkA, TrkA ^G595R, respectively). As a receptor tyrosine kinase (RTK), tropomyosin receptor kinase (Trk) is a key agent target in solid tumors. Trk-IN-11 has the potential for the research of cancer disease .

HY-144423

Trk-IN-10	Trk Receptor	Cancer
Trk-IN-10 (Compound 14j) is a potent inhibitor of TRK (IC₅₀ = 0.86, 6.92 nM, against TrkA, TrkA ^G595R, respectively). As a receptor tyrosine kinase (RTK), tropomyosin receptor kinase (Trk) is a key agent target in solid tumors. Trk-IN-10 (IC₅₀ = 350 nM against ALK) has a higher selectivity of Trk inhibition, which may be of great significance for reducing toxicity .

HY-152208

BPDA2	SHP2	Cancer
BPDA2 is a highly selective and competitive active site SHP2 inhibitor with IC₅₀s of 92.0 nM, 33.39 μM, 40.71 μM for SHP2, SHP1, SHP1B, respectively. DBDA2 downregulates mitogenic and cell survival signaling and RTK expression. BPDA2 suppresses SHP2 mediated signaling and breast cancer cell phenotypes .

HY-149241

SHP2-IN-13	SHP2	Cancer
SHP2-IN-13 is a highly selective and orally active SHP2 “tunnel site” allosteric inhibitor with an IC50 of 83.0 nM. SHP2-IN-13 has the potential for cancers bearing RTK oncogenic drivers and SHP2-related diseases research.

HY-112452

SU11652	VEGFR FGFR PDGFR c-Kit Apoptosis	Cancer
SU11652 is a potent receptor tyrosine kinase (RTK) inhibitor. SU11652 also inhibits several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit. SU11652 can be uesd for spontaneous cancers expressing Kit mutations research .

HY-16961

Sitravatinib 1 Publications Verification MGCD516; MG-516	VEGFR c-Kit FLT3 Discoidin Domain Receptor Trk Receptor	Inflammation/Immunology Cancer
Sitravatinib (MGCD516) is an orally bioavailable receptor tyrosine kinase (RTK) inhibitor with IC₅₀s of 1.5 nM, 2 nM, 2 nM, 5 nM, 6 nM, 6 nM, 8 nM, 0.5 nM, 29 nM, 5 nM, and 9 nM for Axl, MER, VEGFR3, VEGFR2, VEGFR1, KIT, FLT3, DDR2, DDR1, TRKA, TRKB, respectively . Sitravatinib shows potent single-agent antitumor efficacy and enhances the activity of PD-1 blockade through promoting an antitumor immune microenvironment .

HY-16961A

Sitravatinib malate MGCD516 malate; MG-516 malate	VEGFR c-Kit FLT3 Discoidin Domain Receptor Trk Receptor	Inflammation/Immunology Cancer
Sitravatinib malate (MGCD516 malate) is an orally bioavailable receptor tyrosine kinase (RTK) inhibitor with IC₅₀s of 1.5 nM, 2 nM, 2 nM, 5 nM, 6 nM, 6 nM, 8 nM, 0.5 nM, 29 nM, 5 nM, and 9 nM for Axl, MER, VEGFR3, VEGFR2, VEGFR1, KIT, FLT3, DDR2, DDR1, TRKA, TRKB, respectively . Sitravatinib malate shows potent single-agent antitumor efficacy and enhances the activity of PD-1 blockade through promoting an antitumor immune microenvironment .

HY-13892

Dovitinib dilactic acid CHIR-258 dilactic acid; TKI258 dilactic acid	VEGFR	Cancer
Dovitinib (dilactic acid) is an orally active inhibitor of VEGF kinase. Dovitinib (dilactic acid) inhibits receptor tyrosine kinases (RTKs) involved in solid and hematologic cancers and tumor angiogenesis .

HY-146365

HIV-1 inhibitor-30	HIV	Infection Inflammation/Immunology
HIV-1 inhibitor-30 (compound 10i) is a potent HIV-1 inhibitor with an EC₅₀ value of 40 nM and an IC₅₀ value of 80 nM for HIV-1 RT DNA polymerase. HIV-1 inhibitor-30 has highly antiretroviral activity against seven non-nucleoside reverse transcriptase inhibitor (NNRTI)-resistant HIV-1 strains (RT-K103N; RT-Y181C; RT-K103N,Y181C; RT-L100I,K103N; RT-Y188L; RT-K103N,G190A; RT-K103N,V108I) with IC₅₀s of 0.04~1.42 μM. HIV-1 inhibitor-30 can be used for researching AIDS .

HY-153012

Axl/Mer/CSF1R-IN-1

TAM Receptor c-Fms Cancer

Axl/Mer-IN-1 (Compound 1) is an Axl/Mer receptor tyrosine kinase (Axl/Mer RTK) and CSF1R inhibitor with K_ds of <0.1 μM .

Axl/Mer/CSF1R-IN-1	TAM Receptor c-Fms	Cancer
Axl/Mer-IN-1 (Compound 1) is an Axl/Mer receptor tyrosine kinase (Axl/Mer RTK) and CSF1R inhibitor with K_ds of <0.1 μM .

HY-101957

AG 1295 2 Publications Verification	PDGFR	Cardiovascular Disease
AG 1295 is a selective platelet-derived growth factor receptor (PDGFR) tyrosine-kinase inhibitor. AG1295 abolishes autophosphorylation of the PDGFR whereas not affects the autophosphorylation of the EGF receptor .

HY-136173

Batoprotafib 2 Publications Verification TNO155	SHP2 Phosphatase	Cancer
Batoprotafib (TNO155) is a potent selective and orally active allosteric inhibitor of wild-type SHP2 (IC₅₀=0.011 µM). Batoprotafib has the potential for the study of RTK-dependent malignancies, especially advanced solid tumors .

HY-13016S1

Cabozantinib-d4 XL184-d₄; BMS-907351-d₄	VEGFR c-Met/HGFR c-Kit TAM Receptor FLT3 Apoptosis	Cancer
Cabozantinib-d₄ is deuterium labeled Cabozantinib. Cabozantinib is a potent multiple receptor tyrosine kinases (RTKs) inhibitor that inhibits VEGFR2, c-Met, Kit, Axl and Flt3 with IC50s of 0.035, 1.3, 4.6, 7 and 11.3 nM, respectively.

HY-50055

EtDO-P4	Others	Cancer
EtDO-P4 is a nanomolar inhibitor of glycosphingolipid (GSL) synthesis. EtDO-P4 suppresses activation of the EGFR-induced ERK pathway and various receptor tyrosine kinases (RTKs). EtDO-P4 can be used for various types of cancer, including Burkitt’s lymphoma .

HY-10330

Toceranib SU11654; PHA 291639E	PDGFR VEGFR c-Kit	Cancer
Toceranib phosphate (SU11654 phosphate) is an orally active receptor tyrosine kinase (RTK) inhibitor, and it potently inhibits PDGFR, VEGFR, and Kit with K_is of 5 and 6 nM for PDGFRβ and Flk-1/KDR, respectively. Toceranib phosphate (SU11654 phosphate) has antitumor and antiangiogenic activity, and used in the treatment of canine mast cell tumors .

HY-10330A

Toceranib phosphate SU11654 phosphate; PHA 291639E phosphate	PDGFR VEGFR c-Kit	Cancer
Toceranib phosphate (SU11654 phosphate) is an orally active receptor tyrosine kinase (RTK) inhibitor, and it potently inhibits PDGFR, VEGFR, and Kit with K_is of 5 and 6 nM for PDGFRβ and Flk-1/KDR, respectively. Toceranib phosphate (SU11654 phosphate) has antitumor and antiangiogenic activity, and used in the treatment of canine mast cell tumors .

HY-13016S

Cabozantinib-d6 XL184-d₆; BMS-907351-d₆	VEGFR c-Met/HGFR c-Kit TAM Receptor FLT3 Apoptosis	Cancer
Cabozantinib-d₆ is the deuterium labeled Cabozantinib. Cabozantinib is a potent multiple receptor tyrosine kinases (RTKs) inhibitor that inhibits VEGFR2, c-Met, Kit, Axl and Flt3 with IC50s of 0.035, 1.3, 4.6, 7 and 11.3 nM, respectively[1][2][3].

HY-146471

EGFR-IN-51	EGFR Apoptosis	Cancer
EGFR-IN-51 (Compound 6) is a potent EGFR inhibitor with IC₅₀ values of 0.493, 102.60 and 461.63 µM against EGFR, EGFR L858R-TK and EGFR T790M-TK, respectively. EGFR-IN-51 shows cytotoxic activity against cancer cell lines and induces apoptosis .

HY-146472

EGFR-IN-52	EGFR Apoptosis	Cancer
EGFR-IN-52 (Compound 4) is a potent EGFR inhibitor with IC₅₀ values of 0.358, 86.02 and 432.67 µM against EGFR, EGFR L858R-TK and EGFR T790M-TK, respectively. EGFR-IN-52 shows cytotoxic activity against cancer cell lines and induces apoptosis .

HY-10330S

Toceranib-d8	Isotope-Labeled Compounds PDGFR VEGFR c-Kit	Cancer
Toceranib-d₈ is the deuterium labeled Toceranib. Toceranib (SU11654) is an orally active receptor tyrosine kinase (RTK) inhibitor, and it potently inhibits PDGFR, VEGFR, and Kit with Kis of 5 and 6 nM for PDGFRβ and Flk-1/KDR, respectively. Toceranib (SU11654) has antitumor and antiangiogenic activity, and used in the treatment of canine mast cell tumors[1][2].

HY-138696

Zanzalintinib 1 Publications Verification XL092	TAM Receptor c-Met/HGFR VEGFR	Cancer
Zanzalintinib (XL092) is an orally active, ATP-competitive inhibitor of multiple receptor tyrosine kinases (RTKs) including MET, VEGFR2, AXL and MER, with IC₅₀s in cell-based assays of 15 nM, 1.6 nM, 3.4 nM, 7.2 nM respectively. Zanzalintinib exhibits anti-tumor activity. Zanzalintinib has the potential for kinase-dependent diseases and conditions research .

HY-W011266

JNJ-10198409 1 Publications Verification	PDGFR	Cancer
JNJ-10198409 is a relatively selective, orally active, and ATP competitive *PDGF-RTK* (platelet-derived growth factor receptor tyrosine kinase) inhibitor (IC₅₀=2 nM). It is a dual-mechanism, antiangiogenic, and tumor cell antiproliferative agent. JNJ-10198409 has good activity against PDGFR-β kinase (IC₅₀=4.2 nM) and PDGFR-α kinase (IC₅₀=45 nM) .

HY-149510

MET/PDGFRA-IN-1	c-Met/HGFR Apoptosis PDGFR	Cancer
MET/PDGFRA-IN-1 (compound 8c) is a MET and PDGFRA protein inhibitor (IC₅₀: 36 μM for MET). MET/PDGFRA-IN-1 inhibits MET phosphorylation and induces cell apoptosis. MET/PDGFRA-IN-1 inhibits proliferation of MET-positive cells (IC₅₀s: 15.3, 19.0, 22.0, 25.6, 21.0, 31.5 μM for AsPc-1, EBC-1, MKN-45, Mia-Paca-2, HT-29, K562 cells respectively) .

HY-149511

MET/PDGFRA-IN-2	c-Met/HGFR Apoptosis PDGFR	Cancer
MET/PDGFRA-IN-2 (compound 8h) is a MET and PDGFRA protein inhibitor. MET/PDGFRA-IN-2 induces cell apoptosis. MET/PDGFRA-IN-2 inhibits proliferation of MET-positive cells (IC₅₀s: 9.7, 6.1, 12.0, 11.5, 8.6, 34.4 μM for AsPc-1, EBC-1, MKN-45, Mia-Paca-2, HT-29, K562 cells respectively) .

HY-50751

Linifanib 4 Publications Verification ABT-869; AL-39324	PDGFR VEGFR FLT3 c-Fms c-Kit Autophagy Apoptosis	Cancer
Linifanib (ABT-869) is a potent and orally active multi-target inhibitor of VEGFR and PDGFR family with IC₅₀s of 4, 3, 66, and 4 nM for KDR, FLT1, PDGFRβ, and FLT3, respectively. Linifanib shows prominent antitumor activity. Linifanib has much less activity against unrelated RTKs, soluble tyrosine kinases, or serine/threonine kinases. Linifanib is a specific miR-10b inhibitor that blocks miR-10b biogenesis .

HY-12624

Narazaciclib 2 Publications Verification ON123300	CDK AMPK PDGFR	Cancer
Narazaciclib (ON123300), a strong and brain-penetrant multi-kinase inhibitor, inhibits CDK4 (IC₅₀=3.9 nM), Ark5 (IC₅₀=5 nM), PDGFRβ (IC₅₀=26 nM), FGFR1 (IC₅₀=26 nM), RET (IC₅₀=9.2 nM), and FYN (IC₅₀=11 nM). Single agent Narazaciclib causes a dose-dependent suppression of phosphorylation of Akt as well as activation of Erk in brain tumors . Narazaciclib inhibits CDK6 with an IC₅₀ of 9.82 nM .

Cat. No.	Product Name

HY-L016

Protein Tyrosine Kinase Compound Library	1055 compounds
Protein tyrosine kinases (PTKs) are key signaling molecules and important drug targets. Two classes of PTKs are present in cells: the transmembrane receptor PTKs (RTKs) and the nonreceptor PTKs. The RTK family includes the receptors for insulin and for many growth factors, such as EGFR, FGFR, PDGFR, VEGFR, and NGFR. RTKs are transmembrane glycoproteins that are activated by the binding of their ligands, and they transduce the extracellular signal to the cytoplasm by phosphorylating tyrosine residues on the receptors themselves (autophosphorylation) and on downstream signaling proteins. Their principal functions of PTKs involve the regulation of multicellular aspects of the organism. Cell to cell signals concerning growth, differentiation, adhesion, motility, and death are frequently transmitted through tyrosine kinases. In humans, tyrosine kinases have been demonstrated to play significant roles in the development of many disease states, including diabetes and cancers. MCE designs a unique collection of 1055 compounds that act as a useful tool for PTKs-related drug screening and disease research.

Protein Tyrosine Kinase Compound Library

1055 compounds

Protein tyrosine kinases (PTKs) are key signaling molecules and important drug targets. Two classes of PTKs are present in cells: the transmembrane receptor PTKs (RTKs) and the nonreceptor PTKs. The RTK family includes the receptors for insulin and for many growth factors, such as EGFR, FGFR, PDGFR, VEGFR, and NGFR. RTKs are transmembrane glycoproteins that are activated by the binding of their ligands, and they transduce the extracellular signal to the cytoplasm by phosphorylating tyrosine residues on the receptors themselves (autophosphorylation) and on downstream signaling proteins. Their principal functions of PTKs involve the regulation of multicellular aspects of the organism. Cell to cell signals concerning growth, differentiation, adhesion, motility, and death are frequently transmitted through tyrosine kinases. In humans, tyrosine kinases have been demonstrated to play significant roles in the development of many disease states, including diabetes and cancers.

MCE designs a unique collection of 1055 compounds that act as a useful tool for PTKs-related drug screening and disease research.

HY-L015

PI3K/Akt/mTOR Compound Library	568 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 568 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

568 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 568 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.


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Cabozantinib-d6
Cabozantinib-d₆ is the deuterium labeled Cabozantinib. Cabozantinib is a potent multiple receptor tyrosine kinases (RTKs) inhibitor that inhibits VEGFR2, c-Met, Kit, Axl and Flt3 with IC50s of 0.035, 1.3, 4.6, 7 and 11.3 nM, respectively[1][2][3].

Cabozantinib-d4
Cabozantinib-d₄ is deuterium labeled Cabozantinib. Cabozantinib is a potent multiple receptor tyrosine kinases (RTKs) inhibitor that inhibits VEGFR2, c-Met, Kit, Axl and Flt3 with IC50s of 0.035, 1.3, 4.6, 7 and 11.3 nM, respectively.

Toceranib-d8
Toceranib-d₈ is the deuterium labeled Toceranib. Toceranib (SU11654) is an orally active receptor tyrosine kinase (RTK) inhibitor, and it potently inhibits PDGFR, VEGFR, and Kit with Kis of 5 and 6 nM for PDGFRβ and Flk-1/KDR, respectively. Toceranib (SU11654) has antitumor and antiangiogenic activity, and used in the treatment of canine mast cell tumors[1][2].

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