ATP generation

By Targets:	Apoptosis (5) Btk (1) CDK (1) Checkpoint Kinase (Chk) (5) COMT (1) DNA/RNA Synthesis (1) EGFR (1) Isotope-Labeled Compounds (1) Mitochondrial Metabolism (1) Oxidative Phosphorylation (1)
By Research Areas:	Cancer (10) Inflammation/Immunology (1) Neurological Disease (2)

Targets Recommended: ATP Synthase ATP Citrate Lyase P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-144310

DX3-213B	Oxidative Phosphorylation Mitochondrial Metabolism	Cancer
DX3-213B is a highly potent, orally active oxidative phosphorylation (OXPHOS) complex I inhibitor (IC₅₀=3.6 nM). DX3-213B impairs ATP generation (IC₅₀=11 nM), and blocks MIA PaCa-2 cell growth (GI₅₀=11 nM). DX3-213B is used for the research of the pancreatic cancer .

HY-14896

Opicapone 3 Publications Verification BIA 9-1067	COMT	Neurological Disease
Opicapone (BIA 9-1067) is a potent third-generation catechol-O-methyltransferase (COMT) inhibitor for the research of Parkinson's disease and motor fluctuations. Opicapone decreases the ATP content of the cells with an IC₅₀ of 98 μM .

HY-101212

Fadraciclib 5 Publications Verification CYC065	CDK	Cancer
Fadraciclib (CYC065) is a second-generation, orally available ATP-competitive inhibitor of CDK2/CDK9 kinases with IC₅₀s of 5 and 26 nM, respectively .

HY-100213

EAI045 1 Publications Verification	EGFR	Cancer
EAI045 is an allosteric and the fourth-generation inhibitor of mutant EGFR with IC₅₀s of 1.9, 0.019, 0.19 and 0.002 μM for EGFR, EGFR ^L858R, EGFR ^T790M and EGFR ^L858R/T790M at 10 μM ATP, respectively.

HY-107794

Clodronate disodium tetrahydrate Disodium clodronate tetrahydrate	Others	Neurological Disease Inflammation/Immunology Cancer
Clodronate disodium tetrahydrate (Disodium clodronate tetrahydrate) is first-generation bisphosphonate, with anti-osteoporotic, anti-inflammatory and analgesic effects. Clodronate disodium tetrahydrate is a selective, potent, reversible and Cl ^- competitive vesicular nucleotide transporter (VNUT) inhibitor, with an IC₅₀ of 15.6 nM. Clodronate disodium tetrahydrate inhibits vesicular ATP release from neurons and reduces chronic neuropathic and inflammatory pain .

HY-18174

Prexasertib 15+ Cited Publications LY2606368	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib (LY2606368) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib shows potent anti-tumor activity .

HY-18174A

Prexasertib dihydrochloride 15+ Cited Publications LY2606368 dihydrochloride	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib dihydrochloride (LY2606368 dihydrochloride) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib dihydrochloride inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib dihydrochloride causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib dihydrochloride shows potent anti-tumor activity .

HY-18174B

Prexasertib Mesylate Hydrate LY2606368 Mesylate Hydrate; LY2940930	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib Mesylate Hydrate inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib Mesylate Hydrate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib Mesylate Hydrate shows potent anti-tumor activity .

HY-18174C

Prexasertib mesylate LY2606368 mesylate	Checkpoint Kinase (Chk) DNA/RNA Synthesis Apoptosis	Cancer
Prexasertib mesylate (LY2606368 mesylate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib mesylate inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib mesylate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib mesylate shows potent anti-tumor activity .

HY-W757743

Acalabrutinib-d3 ACP-196-d₃	Isotope-Labeled Compounds	Others
Acalabrutinib-d₃ (ACP-196-d₃) is the deuterated form of Acalabrutinib (HY-17600). Acalabrutinib (ACP-196) is an orally active, irreversible, highly selective second-generation BTK inhibitor. Acalabrutinib covalently binds to Cys481 in the ATP-binding pocket of BTK. Acalabrutinib shows strong targeting and efficacy in mouse models of chronic lymphocytic leukemia (CLL).

HY-18174E

Prexasertib dimesylate 15+ Cited Publications LY2606368 dimesylate	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib dimesylate (LY2606368 dimesylate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib dimesylate inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib dimesylate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib dimesylate shows potent anti-tumor activity .

HY-17600

Acalabrutinib Maximum Cited Publications 20 Publications Verification ACP-196	Btk	Cancer
Acalabrutinib (ACP-196) is an orally active, irreversible, and highly selective second-generation BTK inhibitor. Acalabrutinib binds covalently to Cys481 in the ATP-binding pocket of BTK. Acalabrutinib demonstrates potent on-target effects and efficacy in mouse models of chronic lymphocytic leukemia (CLL) . Acalabrutinib is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

Cat. No.	Product Name

HY-L058

Glycolysis Compound Library	689 compounds
Glycolysis is a series of metabolic processes by which one molecule of glucose is catabolized to two molecules of pyruvate with a net gain of two ATP. Glycolysis takes place in 10 steps and catalyzed by a series of enzyme, such as hexokinase, Glucose-6-phosphate isomerase, Phosphofructokinase, etc. Glycolysis is used by all cells in the body for energy generation. Most cancer cells exhibit increased glycolysis and use this metabolic pathway for generation of ATP as a main source of their energy supply. This phenomenon is known as the Warburg effect and is considered as one of the most fundamental metabolic alterations during malignant transformation. Because increased aerobic glycolysis is commonly seen in a wide spectrum of human cancers, development of novel glycolytic inhibitors as a new class of anticancer agents is likely to have broad therapeutic applications. MCE provides a unique collection of 689 glycolysis compounds that mainly target hexokinase, glucokinase, enolase, pyruvate kinase, PDHK, etc. MCE Glycolysis Compound Library is a useful tool for glucose metabolism research and anti-cancer drug discovery.

Glycolysis Compound Library

689 compounds

Glycolysis is a series of metabolic processes by which one molecule of glucose is catabolized to two molecules of pyruvate with a net gain of two ATP. Glycolysis takes place in 10 steps and catalyzed by a series of enzyme, such as hexokinase, Glucose-6-phosphate isomerase, Phosphofructokinase, etc. Glycolysis is used by all cells in the body for energy generation.

Most cancer cells exhibit increased glycolysis and use this metabolic pathway for generation of ATP as a main source of their energy supply. This phenomenon is known as the Warburg effect and is considered as one of the most fundamental metabolic alterations during malignant transformation. Because increased aerobic glycolysis is commonly seen in a wide spectrum of human cancers, development of novel glycolytic inhibitors as a new class of anticancer agents is likely to have broad therapeutic applications.

MCE provides a unique collection of 689 glycolysis compounds that mainly target hexokinase, glucokinase, enolase, pyruvate kinase, PDHK, etc. MCE Glycolysis Compound Library is a useful tool for glucose metabolism research and anti-cancer drug discovery.

Cat. No.	Product Name	Chemical Structure

HY-W757743

Acalabrutinib-d3
Acalabrutinib-d₃ (ACP-196-d₃) is the deuterated form of Acalabrutinib (HY-17600). Acalabrutinib (ACP-196) is an orally active, irreversible, highly selective second-generation BTK inhibitor. Acalabrutinib covalently binds to Cys481 in the ATP-binding pocket of BTK. Acalabrutinib shows strong targeting and efficacy in mouse models of chronic lymphocytic leukemia (CLL).

MCE Japan Authorized Agent ナミキ商事株式会社コスモ・バイオ株式会社
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Inhibitors & Agonists

Screening Libraries

Isotope-Labeled Compounds

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