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Pathways Recommended:	Cell Cycle/DNA Damage Stem Cell/Wnt

Results for "

cell cycle regulation diseases.

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Amyloid-β (3) Apoptosis (3) Bcl-2 Family (1) CDK (1) Epigenetic Reader Domain (1) ERK (1) Isotope-Labeled Compounds (1) JNK (3) NEKs (1) p38 MAPK (3) Reference Standards (1)
By Research Areas:	Cancer (7) Cardiovascular Disease (1) Infection (1) Inflammation/Immunology (2) Neurological Disease (3)

Inhibitors & Agonists

Screening Libraries

Peptides

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: Programmed Cell Death 4 (PDCD4) Itk TOPK NAMPT ALCAM/CD166 GDNF Receptor VISTA BCL6 Tim3 BMI1

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-144425

BSc5367	NEKs	Inflammation/Immunology
BSc5367 is a potent Nek1 inhibitor with an IC₅₀ of 11.5 nM. NIMA-related protein kinase Nek1 is crucially involved in cell cycle regulation, DNA repair and microtubule regulation and dysfunctions of Nek1 play key roles in amyotrophic lateral sclerosis (ALS), polycystic kidney disease (PKD) and several types of radiotherapy resistant cancer .

HY-157486

KMI169	Epigenetic Reader Domain	Cancer
KMI169 is a potent and selective inhibitor targeting lysine methyl-transferase (KMT9) (IC₅₀ = 0.05 μM, K_d = 0.025 μM). KMI169 functions as a bi-substrate inhibitor targeting the cofactor S-5’-adenosyl-L-methionine (SAM) and substrate binding pockets of KMT9. KMI169 can downregulate target genes involved in cell cycle regulation and impair proliferation of tumor cells by inhibiting KMT9. KMI169 is a valuable tool to probe cellular KMT9 functions and can be research for combating diseases including prostate, lung, colon, and invasive bladder cancer .

HY-N7046

Silybin B Silibinin B	Amyloid-β Apoptosis JNK p38 MAPK	Neurological Disease Cancer
Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .

HY-121638B

(E/Z)-CU-3	Bcl-2 Family	Infection Cardiovascular Disease Inflammation/Immunology Cancer
(E/Z)-CU-3 is a MCL-1 modulator. (E/Z)-CU-3 can be used to study hyperproliferative diseases, angiogenic diseases, cell cycle regulation diseases, autophagy regulation diseases, inflammatory diseases and/or infectious diseases .

HY-P10421

PKCδ substrate	ERK	Cancer
PKCδ substrate acts as a nuclear transporter of ERK2 and is involved in ERK2 mediated gene activation. PKCδ is involved in the regulation of cell growth, proliferation, cell cycle arrest, and apoptosis by phosphorylating hBVR and other proteins. PKCδ substrate can be used to study the development of diseases, especially cancer biology .

HY-144175

CDK7-IN-12	CDK	Cancer
CDK7-IN-12 is a potent inhibitor of CDK7. CDK7-IN-12 plays a key role in transcriptional regulation and cell cycle regulation. CDK7-IN-12 effectively inhibit malignant tumor proliferation in vitro and in vivo. CDK7-IN-12 has the potential for the research of cancer disease (extracted from patent WO2021249417A1, compound 43) .

HY-N7046R

Silybin B (Standard) Silibinin B (Standard)	Reference Standards JNK Amyloid-β p38 MAPK Apoptosis	Neurological Disease Cancer
Silybin (Silibinin B) (Standard) is the analytical standard of Silybin B (HY-N7046). This product is intended for research and analytical applications. Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .

HY-N7046S

Silybin B-d3 Silibinin B-d₃	Isotope-Labeled Compounds Amyloid-β Apoptosis JNK p38 MAPK	Neurological Disease Cancer
Silybin B-d₃ (Silibinin B-d₃) is a deuterated Silybin B (HY-N7046). Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .

Cat. No.	Product Name

HY-L012

Metabolism/Protease Compound Library	6,091 compounds
Metabolism is the set of life-sustaining chemical reactions in organisms. Metabolic pathways are enzyme-mediated biochemical reactions that lead to biosynthesis (anabolism) or breakdown (catabolism) of natural product small molecules within a cell or tissue. Acting as catalysts, enzymes are crucial to metabolism - they allow a reaction to proceed more rapidly - and they also allow the regulation of the rate of a metabolic reaction. Proteases are used throughout an organism for various metabolic processes. Proteases control a great variety of physiological processes that are critical for life, including the immune response, cell cycle, cell death, wound healing, food digestion, and protein and organelle recycling. Imbalances in metabolic activities have been found to be critical in a number of pathologies, such as cardiovascular diseases, inflammation, cancer, and neurodegenerative diseases. MCE designs a unique collection of 6,091 Metabolism/Protease-related small molecules that act as a useful tool for drug discovery of metabolism-related diseases.

Metabolism/Protease Compound Library

6,091 compounds

Metabolism is the set of life-sustaining chemical reactions in organisms. Metabolic pathways are enzyme-mediated biochemical reactions that lead to biosynthesis (anabolism) or breakdown (catabolism) of natural product small molecules within a cell or tissue. Acting as catalysts, enzymes are crucial to metabolism - they allow a reaction to proceed more rapidly - and they also allow the regulation of the rate of a metabolic reaction. Proteases are used throughout an organism for various metabolic processes. Proteases control a great variety of physiological processes that are critical for life, including the immune response, cell cycle, cell death, wound healing, food digestion, and protein and organelle recycling. Imbalances in metabolic activities have been found to be critical in a number of pathologies, such as cardiovascular diseases, inflammation, cancer, and neurodegenerative diseases.

MCE designs a unique collection of 6,091 Metabolism/Protease-related small molecules that act as a useful tool for drug discovery of metabolism-related diseases.

HY-L133

Cuproptosis Compound Library	303 compounds
Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis". The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis. Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation and subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress and cell death. Studies have shown that the necessary factors for cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism. Targeted regulation of cuproptosis is a potential choice to treat cancer, rheumatoid arthritis, and other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence and development of tumors by destroying TCA in mitochondria and then inducing cuproptosis. MCE supplies a unique collection of 303 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis and may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, and other diseases.

Cuproptosis Compound Library

303 compounds

Copper is an important co-factor of all biological enzymes, but if the concentration exceeds the threshold of maintaining the homeostasis mechanism, copper will lead to cytotoxicity. This death mechanism has been named "Cuproptosis".

The mechanism of cuproptosis distinct from all other known mechanisms of regulated cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis.

Copper combine with the lipoylated components of the tricarboxylic acid cycle (TCA), leading to lipoylated protein aggregation and subsequent loss of iron-sulfur cluster proteins, ultimately resulting in protein toxicity stress and cell death. Studies have shown that the necessary factors for cuproptosis include the presence of glutathione, mitochondrial metabolism of galactose and pyruvate, and glutamine metabolism.

Targeted regulation of cuproptosis is a potential choice to treat cancer, rheumatoid arthritis, and other diseases. For example, up-regulation of LIPT1 may inhibit the occurrence and development of tumors by destroying TCA in mitochondria and then inducing cuproptosis.

MCE supplies a unique collection of 303 cuproptosis-related compounds, all of which act on the targets or signaling pathways related to cuproptosis and may have in inhibitory or activated effect on cuproptosis. MCE Cuproptosis Library is a useful tool for drug research related to cancer, rheumatoid arthritis, and other diseases.

HY-L050

Ubiquitination Compound Library	362 compounds
Protein ubiquitination is an enzymatic post-translational modification in which an ubiquitin protein is attached to a substrate protein. Ubiquitination involves three main steps: activation, conjugation, and ligation, performed by ubiquitin-activating enzymes (E1s), ubiquitin-conjugating enzymes (E2s), and ubiquitin ligases (E3s), respectively. Ubiquitination affects cellular processes such as apoptosis, cell cycle, DNA damage repair, and membrane transportation, etc. by regulating the degradation of proteins (via the proteasome and lysosome), altering the cellular localization of proteins, affecting proteins activity, and promoting or preventing protein-protein interactions. Deregulation of ubiquitin pathway leads to many diseases such as neurodegeneration, cancer, infection and immunity, etc. MCE offers a unique collection of 362 small molecule modulators with biological activity used for ubiquitination research. Compounds in this library target the key enzymes in ubiquitin pathway. MCE Ubiquitination Compound Library is a useful tool for the research of ubiquitination regulation and the corresponding diseases.

Ubiquitination Compound Library

362 compounds

Protein ubiquitination is an enzymatic post-translational modification in which an ubiquitin protein is attached to a substrate protein. Ubiquitination involves three main steps: activation, conjugation, and ligation, performed by ubiquitin-activating enzymes (E1s), ubiquitin-conjugating enzymes (E2s), and ubiquitin ligases (E3s), respectively. Ubiquitination affects cellular processes such as apoptosis, cell cycle, DNA damage repair, and membrane transportation, etc. by regulating the degradation of proteins (via the proteasome and lysosome), altering the cellular localization of proteins, affecting proteins activity, and promoting or preventing protein-protein interactions. Deregulation of ubiquitin pathway leads to many diseases such as neurodegeneration, cancer, infection and immunity, etc.

MCE offers a unique collection of 362 small molecule modulators with biological activity used for ubiquitination research. Compounds in this library target the key enzymes in ubiquitin pathway. MCE Ubiquitination Compound Library is a useful tool for the research of ubiquitination regulation and the corresponding diseases.

Cat. No.	Product Name	Target	Research Area

HY-P10421

PKCδ substrate	ERK	Cancer
PKCδ substrate acts as a nuclear transporter of ERK2 and is involved in ERK2 mediated gene activation. PKCδ is involved in the regulation of cell growth, proliferation, cell cycle arrest, and apoptosis by phosphorylating hBVR and other proteins. PKCδ substrate can be used to study the development of diseases, especially cancer biology .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N7046

Silybin B Silibinin B	Flavanonols Structural Classification Flavonoids Glycine soya Source classification Phenols Polyphenols Cyamopsis tetragonoloba (L.) Taub. Plants Compositae	Amyloid-β Apoptosis JNK p38 MAPK
Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .

HY-N7046R

Silybin B (Standard) Silibinin B (Standard)	Flavanonols Structural Classification Flavonoids Glycine soya Source classification Phenols Polyphenols Cyamopsis tetragonoloba (L.) Taub. Plants Compositae	Reference Standards JNK Amyloid-β p38 MAPK Apoptosis
Silybin (Silibinin B) (Standard) is the analytical standard of Silybin B (HY-N7046). This product is intended for research and analytical applications. Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .

Cat. No.	Product Name	Chemical Structure

HY-N7046S

Silybin B-d3
Silybin B-d₃ (Silibinin B-d₃) is a deuterated Silybin B (HY-N7046). Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .

Silybin B-d3

Silybin B-d₃ (Silibinin B-d₃) is a deuterated Silybin B (HY-N7046). Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .

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cell cycle regulation diseases.

Inhibitors & Agonists

Screening Libraries

Peptides

NaturalProducts

Isotope-Labeled Compounds

Natural
Products