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Pathways Recommended:	Protein Tyrosine Kinase/RTK

Results for "

tyrosine autophosphorylation

" in MedChemExpress (MCE) Product Catalog:

By Targets:	FLT3 (6) Apoptosis (17) Autophagy (16) Bcr-Abl (2) c-Kit (1) Caspase (2) CDK (1) Drug Metabolite (2) EGFR (16) FGFR (3) Fungal (1) Insulin Receptor (1) IRE1 (6) Isotope-Labeled Compounds (3) JAK (1) Ligands for Target Protein for PROTAC (2) Mitophagy (6) PDGFR (11) Phosphatase (2) SARS-CoV (1) Src (3) TGF-β Receptor (1) VEGFR (7)
By Research Areas:	Cancer (33) Cardiovascular Disease (3) Infection (1) Inflammation/Immunology (1) Metabolic Disease (1)
Click Chemistry:	Alkynes (2)

Inhibitors & Agonists

Screening Libraries

Peptides

Natural
Products

Isotope-Labeled Compounds

Click Chemistry

Targets Recommended: Btk Syk DYRK Pyk2 BRK FAK FLT3 Anaplastic lymphoma kinase (ALK)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-100434

PD-161570	FGFR PDGFR EGFR Src TGF-β Receptor	Cardiovascular Disease Cancer
PD-161570 is a potent and ATP-competitive human FGF-1 receptor inhibitor with an IC₅₀ of 39.9 nM and a K_i of 42 nM. PD-161570 also inhibits the PDGFR, EGFR and *c-Src tyrosine* kinases with IC₅₀ values of 310 nM, 240 nM, and 44 nM, respectively. PD-161570 inhibits PDGF*-stimulated autophosphorylation* and FGF-1 receptor phosphorylation with IC₅₀s of 450 nM and 622 nM, respectively . PD-161570 is also a bone morphogenetic proteins (BMPs) and TGF-β signaling inhibitor .

HY-107594

Benzene hexabromide	JAK	Cancer
Benzene hexabromide, a bromohydrocarbon, is a potent inhibitor of JAK2 tyrosine kinase autophosphorylation.

HY-101429

RG13022 Tyrphostin RG13022	EGFR	Cancer
RG13022 is a tyrosine kinase inhibitor; inhibits the autophosphorylation reaction of the EGF receptor with an IC₅₀ of 4 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-101962

HNMPA	Insulin Receptor	Metabolic Disease
HNMPA is a membrane impermeable *insulin receptor tyrosine* kinase** inhibitor. HNMPA inhibits serine and tyrosine autophosphorylation by the human insulin receptor. HNMPA has no effect on protein kinase C or cyclic AMP-dependent protein kinase activities

HY-10255A

Sunitinib 45+ Cited Publications SU 11248	VEGFR PDGFR IRE1 Mitophagy Autophagy Apoptosis	Cancer
Sunitinib (SU 11248) is a multi-targeted receptor tyrosine kinase inhibitor with IC₅₀s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively . Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation .

HY-10255

Sunitinib Malate 45+ Cited Publications SU 11248 Malate	PDGFR VEGFR IRE1 Mitophagy Autophagy Apoptosis	Cancer
Sunitinib Malate (SU 11248 Malate) is a multi-targeted receptor tyrosine kinase inhibitor with IC₅₀s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively . Sunitinib Malate, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation .

HY-10255AS

Sunitinib-d10 SU 11248-d₁₀	VEGFR PDGFR IRE1 Mitophagy Autophagy Apoptosis	Cancer
Sunitinib-d₁₀ is a deuterium labeled Sunitinib. Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor with IC50s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively[1]. Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation[2].

HY-10255AS1

Sunitinib-d4	Isotope-Labeled Compounds VEGFR PDGFR IRE1 Mitophagy Autophagy Apoptosis	Cancer
Sunitinib-d₄ is the deuterium labeled Sunitinib. Sunitinib (SU 11248) is a multi-targeted receptor tyrosine kinase inhibitor with IC50s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively[1]. Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation[2].

HY-10255AR

Sunitinib (Standard)	VEGFR PDGFR IRE1 Mitophagy Autophagy Apoptosis	Cancer
Sunitinib (Standard) is the analytical standard of Sunitinib. This product is intended for research and analytical applications. Sunitinib (SU 11248) is a multi-targeted receptor tyrosine kinase inhibitor with IC₅₀s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively . Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation .

HY-10255R

Sunitinib Malate (Standard)	PDGFR VEGFR IRE1 Mitophagy Autophagy Apoptosis	Cancer
Sunitinib (Malate) (Standard) is the analytical standard of Sunitinib (Malate). This product is intended for research and analytical applications. Sunitinib Malate (SU 11248 Malate) is a multi-targeted receptor tyrosine kinase inhibitor with IC₅₀s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively . Sunitinib Malate, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation .

HY-15463S1

Imatinib-d4 STI571 d₄; CGP-57148B d₄	Bcr-Abl PDGFR c-Kit SARS-CoV Autophagy	Cancer
Imatinib-d₄ is a deuterium labeled Imatinib (STI571). Imatinib is an orally bioavailable tyrosine kinases inhibitor that selectively inhibits BCR/ABL, v-Abl, PDGFR and c-kit kinase activity[1][2].

HY-116111

AG 370	PDGFR	Cardiovascular Disease
AG 370, an indole tyrphostin, is a potent PDGF-induced mitogenesis inhibotor (IC₅₀ of 20 μM). AG 370 displays weak inhibition of the EGF receptor .

HY-P1799

[pTyr5] EGFR (988-993)	Phosphatase	Others
[pTyr5] EGFR (988-993) is derived from the autophosphorylation site (Tyr992) of epidermal growth factor receptor (EGFR 988-993). [pTyr5] EGFR (988-993) is often complexed with the catalytically inactive protein-tyrosine phosphate 1B (PTP1B) .

HY-P1799A

[pTyr5] EGFR (988-993) (TFA)	Phosphatase	Others
[pTyr5] EGFR (988-993) TFA is derived from the autophosphorylation site (Tyr992) of epidermal growth factor receptor (EGFR 988-993). [pTyr5] EGFR (988-993) TFA is often complexed with the catalytically inactive protein-tyrosine phosphate 1B (PTP1B) .

HY-50895A

Gefitinib hydrochloride Maximum Cited Publications 119 Publications Verification ZD-1839 hydrochloride	EGFR	Cancer
Gefitinib hydrochloride (ZD1839 hydrochloride) is a potent, selective and orally active *EGFR tyrosine* kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib hydrochloride selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and that blocks EGF-stimulated EGFR** autophosphorylation in tumor cells. Gefitinib hydrochloride also induces autophagy. Gefitinib hydrochloride has antitumour activity .

HY-118304

AKN-028	FLT3 Apoptosis Caspase	Cancer
AKN-028, a novel tyrosine kinase (TK) inhibitor, is a potent, orally active *FMS-like receptor tyrosine* kinase 3 (FLT3) inhibitor with an IC₅₀** value of 6 nM. AKN-028 inhibits FLT3 autophosphorylation. AKN-028 induces dose-dependent cytotoxic response (mean IC₅₀=1 μM). AKN-028 induces apoptosisby activation of caspase 3. AKN-028 can be used in research of acute myeloid leukemia (AML) .

HY-118304B

AKN-028 acetate	FLT3 Apoptosis Caspase	Cancer
AKN-028 acetate, a novel tyrosine kinase (TK) inhibitor, is a potent, orally active FMS-like receptor tyrosine kinase 3 (FLT3) inhibitor with an IC50 value of 6 nM. AKN-028 acetate inhibits FLT3 autophosphorylation. AKN-028 acetate induces dose-dependent cytotoxic response (mean IC50=1 μM). AKN-028 acetate induces apoptosisby activation of caspase 3. AKN-028 acetate can be used in research of acute myeloid leukemia (AML).

HY-14674

CP-724714 3 Publications Verification	EGFR Apoptosis	Cancer
CP-724714 is a potent, selective and orally active ErbB2 (HER2) tyrosine kinase inhibitor, with an IC₅₀ of 10 nM. CP-724714 displays a marked selectivity against EGFR kinase (IC₅₀=6400 nM). CP-724714 potently inhibits ErbB2 receptor autophosphorylation in intact cells. Antitumor activities .

HY-108263

3-Hydroxy Midostaurin CGP52421	FLT3	Cancer
3-Hydroxy Midostaurin (CGP 52421), a metabolite of PKC412, effectively inhibits *FMS-like tyrosine* kinase-3 (FLT3)** autophosphorylation with IC₅₀s of approximately 132 nM and 9.8 μM in culture medium and plasma, respectively. 3-Hydroxy Midostaurin is less selective but more cytotoxic than PKC412 .

HY-131257

Gefitinib impurity 1	Drug Metabolite	Others
Gefitinib impurity 1 is the impurity of Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active *EGFR tyrosine* kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and that blocks EGF-stimulated EGFR** autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity .

HY-133779

Gefitinib impurity 5	Drug Metabolite	Others
Gefitinib impurity 5 is the impurity of Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active *EGFR tyrosine* kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and that blocks EGF-stimulated EGFR** autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity .

HY-108263S

3-Hydroxy Midostaurin-d5 CGP52421-d₅	Isotope-Labeled Compounds FLT3	Cancer
3-Hydroxy Midostaurin-d₅ is a deuterium labeled 3-Hydroxy Midostaurin. 3-Hydroxy Midostaurin is a metabolite of PKC412, which effectively inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation with IC50s of approximately 132 nM and 9.8 μM in culture medium and plasma, respectively[1].

HY-112345

PD-089828	FGFR PDGFR EGFR Src	Cancer
PD-089828 is an ATP competitive inhibitor of FGFR-1, PDGFR-β and EGFR (IC₅₀s=0.15, 1.76, and 5.47 µM, respectively) and a noncompetitive inhibitor of c-Src tyrosine kinase (IC₅₀=0.18 µM). PD-089828 also inhibits MAPK with an IC₅₀ of 7.1 µM. PD-089828 inhibits PDGF-, EGF- and bFGF-mediated tyrosine kinase receptor autophosphorylation in vitro. PD-089828 has a long-lasting cellular activity .

HY-50895

Gefitinib Maximum Cited Publications 119 Publications Verification ZD1839	EGFR Autophagy Apoptosis	Cancer
Gefitinib (ZD1839) is a potent, selective and orally active *EGFR tyrosine* kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and that blocks EGF-stimulated EGFR** autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .

HY-100663

Gefitinib impurity 2	EGFR	Others
Gefitinib impurity 2 is the impurity of Gefitinib. Gefitinib (ZD1839; HY-50895) is a potent, selective and orally active *EGFR tyrosine* kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and that blocks EGF-stimulated EGFR** autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity .

HY-50895S1

Gefitinib-d6 ZD1839-d₆	EGFR Autophagy	Cancer
Gefitinib-d₆ is the deuterium labeled Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity[1][2].

HY-50895B

Gefitinib dihydrochloride ZD 1839 dihydrochloride	EGFR Autophagy Apoptosis	Cancer
Gefitinib (ZD 1839) dihydrochloride is a potent, selective and orally active *EGFR tyrosine* kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib dihydrochloride selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and blocks EGF-stimulated EGFR** autophosphorylation in tumor cells. Gefitinib dihydrochloride also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .

HY-50896

Erlotinib 80+ Cited Publications CP-358774; NSC 718781; OSI-774	EGFR Autophagy	Cancer
Erlotinib (CP-358774) is a directly acting EGFR tyrosine kinase inhibitor, with an IC₅₀ of 2 nM for human EGFR. Erlotinib reduces EGFR autophosphorylation in intact tumor cells with an IC₅₀ of 20 nM. Erlotinib is used for the treatment of non-small cell lung cancer . Erlotinib is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

HY-50896S

Erlotinib-d6 CP-358774-d₆; NSC 718781-d₆; OSI-774-d₆	EGFR	Cancer
Erlotinib-d₆ (CP-358774 D6) is a deuterium labeled Erlotinib (CP-358774). Erlotinib is a directly acting inhibitor EGFR tyrosine kinase inhibitor with an IC50 of 2 nM for human EGFR[1]. Erlotinib-d6 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-50895S2

Gefitinib-d3	Isotope-Labeled Compounds EGFR Autophagy	Cancer
Gefitinib-d₃ (ZD1839-d3) is the deuterium labeled Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity[1][2].

HY-156618

Irpagratinib ABSK011	FGFR	Cancer
Irpagratinib (ABSK011) is an orally active inhibitor of fibroblast growth factor receptor (FGFR) tyrosine kinase, targeting to FGFR4 (IC50<10 nM). Irpagratinib inhibits the auto-phosphorylation of FGFR4 and blocks signal transduction from FGFR4 to downstream pathway activation. Irpagratinib exhibits high exposure in PK study in mouse, rat and dog, and also shows antineoplastic/anti-tumor activity in subcutaneous xenograft tumor models .

HY-108485

Damnacanthal	Src Apoptosis Fungal	Infection Inflammation/Immunology Cancer
Damnacanthal is an anthraquinone isolated from the root of Morinda citrifolia. Damnacanthal is a highly potent, selective inhibitor of *p56 ^lck tyrosine* kinase activity. Natural Damnacanthal inhibits p56 ^lck** autophosphorylation and phosphorylation of exogenous substrates with IC₅₀s of 46 nM and 220 nM, respectively. Damnacanthal is a potent inducer of apoptosis with anticancer activity. Damnacanthal also has antinociceptive, anti-inflammatory effects in mice and anti-fungal activity against *Candida albicans* .

HY-116624

MAZ51 3 Publications Verification	VEGFR Apoptosis	Cancer
MAZ51 is a selective inhibitor of VEGFR-3 (Flt-4) tyrosine kinase. MAZ51 inhibits VEGF-C-induced activation of VEGFR-3 without blocking VEGF-C-mediated stimulation of VEGFR2. MAZ51 had no effect on ligand-induced autophosphorylation of EGFR, IGF-1R and PDGFRβ. MAZ51 blocks proliferation and induces apoptosis in a wide variety of tumor cells. Antitumor activity .

HY-101042

AG-494 Tyrphostin AG 494	EGFR CDK	Cancer
AG-494 (Tyrphostin AG 494) is a potent and selective EGFR tyrosine kinase inhibitor (IC₅₀=0.7 μM). AG-494 inhibits the autophosphorylation of EGFR, ErbB2, HER1-2 and PDGF-R with IC₅₀s 1.1, 39, 45 and 6 μM, respectively. AG-494 blocks Cdk2 activation and inhibits EGF-dependent DNA synthesis .

HY-50895R

Gefitinib (Standard) ZD1839 (Standard)	EGFR Autophagy Apoptosis	Cancer
Gefitinib (Standard) is the analytical standard of Gefitinib. This product is intended for research and analytical applications. Gefitinib (ZD1839) is a potent, selective and orally active *EGFR tyrosine* kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and that blocks EGF-stimulated EGFR** autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .

HY-17499

EGFR-IN-12	EGFR Apoptosis	Cancer
EGFR-IN-12 is a 4,6-disubstituted pyrimidine and is a potent, ATP-competitive, irreversible and highly selective EGFR inhibitor with an IC₅₀of 21 nM. EGFR-IN-12 also inhibits mutant EGFR ^L858R and EGFR ^L861Q with IC₅₀s of 63 nM and 4 nM, respectively. EGFR-IN-12 displays strong selectivity for EGFR over HER4 (IC₅₀ = 7640 nM) and a panel of 55 other kinases. EGFR-IN-12 induces cells apoptosis and has antitumor activity .

HY-13001

Quizartinib 25+ Cited Publications AC220	FLT3 Ligands for Target Protein for PROTAC Apoptosis Autophagy	Cancer
Quizartinib (AC220) is an orally active, highly selective and potent second-generation type II *FLT3 tyrosine* kinase inhibitor, with a K_d** of 1.6 nM. Quizartinib inhibits wild-type FLT3 and FLT3-ITD autophosphorylation in MV4-11 cells with IC₅₀s of 4.2 and 1.1 nM, respectively. Quizartinib can be linked to the VHL ligand via an optimized linker to form a PROTAC FLT3 degrader. Quizartinib induces apoptosis .

HY-50896R

Erlotinib (Standard)	EGFR Autophagy	Cancer
Erlotinib (Standard) is the analytical standard of Erlotinib. This product is intended for research and analytical applications. Erlotinib (CP-358774) is a directly acting EGFR tyrosine kinase inhibitor, with an IC₅₀ of 2 nM for human EGFR. Erlotinib reduces EGFR autophosphorylation in intact tumor cells with an IC₅₀ of 20 nM. Erlotinib is used for the treatment of non-small cell lung cancer . Erlotinib is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

HY-13001R

Quizartinib (Standard)	FLT3 Ligands for Target Protein for PROTAC Apoptosis Autophagy	Cancer
Quizartinib (Standard) is the analytical standard of Quizartinib. This product is intended for research and analytical applications. Quizartinib (AC220) is an orally active, highly selective and potent second-generation type II *FLT3 tyrosine* kinase inhibitor, with a K_d** of 1.6 nM. Quizartinib inhibits wild-type FLT3 and FLT3-ITD autophosphorylation in MV4-11 cells with IC₅₀s of 4.2 and 1.1 nM, respectively. Quizartinib can be linked to the VHL ligand via an optimized linker to form a PROTAC FLT3 degrader. Quizartinib induces apoptosis .

HY-147414

Vamotinib PF-114	Bcr-Abl	Cancer
Vamotinib (PF-114) is a potent, selective and orally active tyrosine kinase inhibitor. Vamotinib inhibits the autophosphorylation of BCR/ABL and BCR/ABL-T315I. Vamotinib induces apoptosis. Vamotinib shows anti-proliferative and anti-tumor activity. Vamotinib has the potential for the research of resistant philadelphia chromosome-positive (Ph+) leukemia. Vamotinib inhibits ABL series kinases with IC₅₀s of 0.49 nM (ABL), 0.78 nM (ABL ^T315I), 9.5 nM (ABL ^E255K), 2.0 nM (ABL ^F317I), 7.4 nM (ABL ^G250E), 1.0 nM (ABL ^H396P), 2.8 nM (ABL ^M351T), 12 nM (ABL ^Q252H), and 4.1 nM (ABL ^Y253F), respectively . Vamotinib is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

Cat. No.	Product Name

HY-L016

Protein Tyrosine Kinase Compound Library	1,076 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 1,076 compounds that act as a useful tool for PTKs-related drug screening and disease research.

Protein Tyrosine Kinase Compound Library

1,076 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 1,076 compounds that act as a useful tool for PTKs-related drug screening and disease research.

Cat. No.	Product Name	Target	Research Area

HY-P1799

[pTyr5] EGFR (988-993)	Phosphatase	Others
[pTyr5] EGFR (988-993) is derived from the autophosphorylation site (Tyr992) of epidermal growth factor receptor (EGFR 988-993). [pTyr5] EGFR (988-993) is often complexed with the catalytically inactive protein-tyrosine phosphate 1B (PTP1B) .

HY-P1799A

[pTyr5] EGFR (988-993) (TFA)	Phosphatase	Others
[pTyr5] EGFR (988-993) TFA is derived from the autophosphorylation site (Tyr992) of epidermal growth factor receptor (EGFR 988-993). [pTyr5] EGFR (988-993) TFA is often complexed with the catalytically inactive protein-tyrosine phosphate 1B (PTP1B) .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-108485

Damnacanthal	Structural Classification Classification of Application Fields Source classification Plants Infection Quinones Monophenols Anthraquinones Rubiaceae Morinda citrifolia Linn. Phenols Inflammation/Immunology Disease Research Fields	Src Apoptosis Fungal
Damnacanthal is an anthraquinone isolated from the root of Morinda citrifolia. Damnacanthal is a highly potent, selective inhibitor of *p56 ^lck tyrosine* kinase activity. Natural Damnacanthal inhibits p56 ^lck** autophosphorylation and phosphorylation of exogenous substrates with IC₅₀s of 46 nM and 220 nM, respectively. Damnacanthal is a potent inducer of apoptosis with anticancer activity. Damnacanthal also has antinociceptive, anti-inflammatory effects in mice and anti-fungal activity against *Candida albicans* .

Cat. No.	Product Name	Chemical Structure

HY-10255AS

Sunitinib-d10
Sunitinib-d₁₀ is a deuterium labeled Sunitinib. Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor with IC50s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively[1]. Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation[2].

HY-15463S1

Imatinib-d4
Imatinib-d₄ is a deuterium labeled Imatinib (STI571). Imatinib is an orally bioavailable tyrosine kinases inhibitor that selectively inhibits BCR/ABL, v-Abl, PDGFR and c-kit kinase activity[1][2].

HY-50895S1

Gefitinib-d6
Gefitinib-d₆ is the deuterium labeled Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity[1][2].

HY-10255AS1

Sunitinib-d4
Sunitinib-d₄ is the deuterium labeled Sunitinib. Sunitinib (SU 11248) is a multi-targeted receptor tyrosine kinase inhibitor with IC50s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively[1]. Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation[2].

HY-108263S

3-Hydroxy Midostaurin-d5
3-Hydroxy Midostaurin-d₅ is a deuterium labeled 3-Hydroxy Midostaurin. 3-Hydroxy Midostaurin is a metabolite of PKC412, which effectively inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation with IC50s of approximately 132 nM and 9.8 μM in culture medium and plasma, respectively[1].

HY-50896S

Erlotinib-d6
Erlotinib-d₆ (CP-358774 D6) is a deuterium labeled Erlotinib (CP-358774). Erlotinib is a directly acting inhibitor EGFR tyrosine kinase inhibitor with an IC50 of 2 nM for human EGFR[1]. Erlotinib-d6 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-50895S2

Gefitinib-d3

Gefitinib-d₃ (ZD1839-d3) is the deuterium labeled Gefitinib. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy. Gefitinib has antitumour activity[1][2].

Cat. No.	Product Name		Classification

HY-50896

Erlotinib 80+ Cited Publications CP-358774; NSC 718781; OSI-774		Alkynes
Erlotinib (CP-358774) is a directly acting EGFR tyrosine kinase inhibitor, with an IC₅₀ of 2 nM for human EGFR. Erlotinib reduces EGFR autophosphorylation in intact tumor cells with an IC₅₀ of 20 nM. Erlotinib is used for the treatment of non-small cell lung cancer . Erlotinib is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

HY-50896S

Erlotinib-d6 CP-358774-d₆; NSC 718781-d₆; OSI-774-d₆		Alkynes
Erlotinib-d₆ (CP-358774 D6) is a deuterium labeled Erlotinib (CP-358774). Erlotinib is a directly acting inhibitor EGFR tyrosine kinase inhibitor with an IC50 of 2 nM for human EGFR[1]. Erlotinib-d6 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

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tyrosine autophosphorylation

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