Search Result

Pathways Recommended:	Cell Cycle/DNA Damage

Results for "

DNA damage repair

" in MedChemExpress (MCE) Product Catalog:

By Targets:	DNA Alkylator/Crosslinker (2) DNA/RNA Synthesis (6) Adenosine Deaminase (1) Akt (1) Apoptosis (14) ATM/ATR (5) c-Kit (2) c-Met/HGFR (2) CDK (2) Drug Metabolite (2) Endogenous Metabolite (2) Epigenetic Reader Domain (2) ERK (1) FLAP (2) FLT3 (2) HDAC (2) mTOR (1) PARP (12) PDGFR (2) Phosphodiesterase (PDE) (1) PROTACs (1) RAD51 (3) RET (2) Ribosomal S6 Kinase (RSK) (1) Separase (1) Sirtuin (1) Thyroid Hormone Receptor (1) VEGFR (1)
By Research Areas:	Cancer (39) Cardiovascular Disease (1) Endocrinology (1) Inflammation/Immunology (1) Metabolic Disease (1) Neurological Disease (2)

By Targets:

DNA Alkylator/Crosslinker (2)

DNA/RNA Synthesis (6)

Adenosine Deaminase (1)

Akt (1)

Apoptosis (14)

ATM/ATR (5)

c-Kit (2)

c-Met/HGFR (2)

CDK (2)

Drug Metabolite (2)

Endogenous Metabolite (2)

Epigenetic Reader Domain (2)

ERK (1)

FLAP (2)

FLT3 (2)

HDAC (2)

mTOR (1)

PARP (12)

PDGFR (2)

Phosphodiesterase (PDE) (1)

PROTACs (1)

RAD51 (3)

RET (2)

Ribosomal S6 Kinase (RSK) (1)

Separase (1)

Sirtuin (1)

Thyroid Hormone Receptor (1)

VEGFR (1)

By Research Areas:

Cancer (39)

Cardiovascular Disease (1)

Endocrinology (1)

Inflammation/Immunology (1)

Metabolic Disease (1)

Neurological Disease (2)

Inhibitors & Agonists

Screening Libraries

Biochemical Assay Reagents

Peptides

Natural
Products

Targets Recommended: DNA-PK DNA Methyltransferase DNA Stain DNA Alkylator/Crosslinker DNA/RNA Synthesis

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-Q04764

TI17	Thyroid Hormone Receptor Apoptosis	Cancer
TI17 is an inhibitor of the thyroid hormone receptor-interacting protein Trip13 and has anticancer activity. TI17 effectively inhibits multiple myeloma (MM) cell proliferation and induces cell cycle arrest and apoptosis. Trip13 is an AAA-ATPase that mediates double-strand break (DSB) repair; TI17 inhibits Trip13 function and increases DNA damage .

HY-108708

GeA-69	PARP	Cancer
GeA-69 is a selective, allosteric inhibitor of poly-adenosine-diphosphate-ribose polymerase 14 (PARP14) targeting macrodomain 2 (MD2), with a K_d value of 2.1 µM. GeA-69 involves in DNA damage repair mechanisms and prevents recruitment of PARP14 MD2 to sites of laser-induced DNA damage .

HY-P5265

Tetrapeptide	DNA/RNA Synthesis	Metabolic Disease
Tetrapeptide, an analogue of α-MSH, induces melanin synthesis. Tetrapeptide diminishes DNA damage by reducing the production of reactive oxidative species and enhancing repair of DNA photoproducts .

HY-155348

Ru3	PARP	Cancer
Ru3 is a poly(ADP-ribose) polymerase 1 inhibitor. Ru3 induces apoptosisin MCF-7 cells by multiple modes, inclusive of inducing DNA damage, suppressing DNA damage repair, disturbing cell cycle distribution, decreasing the mitochondrial membrane potential, and increasing the intracellular reactive oxygen species levels .

HY-142671

ATR-IN-5	ATM/ATR	Cancer
ATR-IN-5 is a potent inhibitor of ATR. ATR is a class of protein kinases involved in genome stability and DNA damage repair, and is a member of the PIKK family. ATR-IN-5 has the potential for the research of ATR kinase-mediated diseases such as proliferative diseases and cancer (extracted from patent CN112047938A, compound D24) .

HY-114842

TDRL-551	Others	Cancer
TDRL-551 is a potent replication protein A (RPA) inhibitor (IC₅₀=18 µM). TDRL-551 inhibits RPA-DNA interaction and increases the efficacy of Platinum (Pt)-based chemotherapy in lung and ovarian cancer. RPA plays essential roles in both nucleotide excision repair (NER) and homologous recombination (HR), along with its role in DNA replication and DNA damage checkpoint activation .

HY-142672

ATR-IN-6	ATM/ATR	Cancer
ATR-IN-6 is a potent inhibitor of ATR. ATR is a class of protein kinases involved in genome stability and DNA damage repair, and is a member of the PIKK family. ATR-IN-6 has the potential for the research of ATR kinase-mediated diseases such as proliferative diseases and cancer (extracted from patent WO2021233376A1, compound A22) .

HY-135218

AV-153	DNA/RNA Synthesis	Cancer
AV-153, a 1,4-dihydropyridine (1,4-DHP) derivative, is an antimutagenic. AV-153 intercalates to *DNA* in a single strand break and reduces DNA damage, stimulates DNA repair in human cells in vitro. AV-153 interacts with thymine and cytosine and has an influence on poly(ADP)ribosylation. AV-153 has anti-cancer activity .

HY-135218A

AV-153 free base 1 Publications Verification	DNA/RNA Synthesis	Cancer
AV-153 free base, a 1,4-dihydropyridine (1,4-DHP) derivative, is an antimutagenic. AV-153 free base intercalates to *DNA* in a single strand break and reduces DNA damage, stimulates DNA repair in human cells in vitro. AV-153 free base interacts with thymine and cytosine and has an influence on poly(ADP)ribosylation. AV-153 free base has anti-cancer activity .

HY-144874

AZ3391	PARP	Neurological Disease Cancer
AZ3391 is a potent inhibitor of PARP. AZ3391 is a quinoxaline derivative. PARP family of enzymes play an important role in a number of cellular processes, such as replication, recombination, chromatin remodeling, and DNA damage repair. AZ3391 has the potential for the research of diseases and conditions occurring in tissues in the central nervous system, such as the brain and spinal cord (extracted from patent WO2021260092A1, compound 23) .

HY-113306

1-Methyladenine

Endogenous Metabolite Others

1-Methyladenine is a product of alkylation damage in DNA which can be repaired by damage reversal by oxidative demethylation.

1-Methyladenine	Endogenous Metabolite	Others
1-Methyladenine is a product of alkylation damage in DNA which can be repaired by damage reversal by oxidative demethylation.

HY-100016

AZD0156 5+ Cited Publications	ATM/ATR Apoptosis	Cancer
AZD0156 is a potent, selective and orally active ATM inhibitor with an IC₅₀ of 0.58 nM. AZD0156 inhibits the ATM-mediated signaling, prevents DNA damage checkpoint activation, disrupts DNA damage repair, and induces tumor cell apoptosis .

HY-10206

Amuvatinib 5+ Cited Publications MP470; HPK 56	c-Kit PDGFR RAD51 FLT3 c-Met/HGFR RET Apoptosis	Cancer
Amuvatinib (MP470) is an orally bioavailable multi-targeted tyrosine kinase inhibitor with potent activity against mutant c-Kit, PDGFRα, Flt3, c-Met and c-Ret. Amuvatinib (MP470) is also a DNA repair suppressor through suppression of DNA repair protein RAD51, thereby disrupting DNA damage repair . Antineoplastic activity .

HY-10206A

Amuvatinib hydrochloride MP470 hydrochloride; HPK 56 hydrochloride	c-Kit PDGFR RAD51 FLT3 c-Met/HGFR RET	Cancer
Amuvatinib hydrochloride (MP470 hydrochloride) is an orally bioavailable multi-targeted tyrosine kinase inhibitor with potent activity against mutant c-Kit, PDGFRα, Flt3, c-Met and c-Ret. Amuvatinib hydrochloride (MP470 hydrochloride) is also a DNA repair suppressor through suppression of DNA repair protein RAD51, thereby disrupting DNA damage repair . Antineoplastic activity .

HY-155595

SNM1A-IN-1

Others Others

SNM1A-IN-1 (compound 11a) is an inhibtor of SNM1A (a DNA damage repair enzyme with cytotoxicity) .

SNM1A-IN-1	Others	Others
SNM1A-IN-1 (compound 11a) is an inhibtor of SNM1A (a DNA damage repair enzyme with cytotoxicity) .

HY-123401

DDRI-18	DNA/RNA Synthesis	Cancer
DDRI-18 is a DNA damage response inhibitor that inhibits the non-homologous end-joining (NHEJ) DNA repair process. DDRI-18 is an effective chemosensitizing agent .

HY-113064

Selenocystine	Endogenous Metabolite	Cancer
Selenocystine is a broad-spectrum anti-cancer agent. Selenocystine induces DNA damage in HepG2 cells, particularly in the form of DNA double strand breaks (DSBs). Selenocystine exhibits great promise as a therapeutic or adjuvant agent targeting DNA repair for cancer treatment .

HY-D0836

EDTA dipotassium dihydrate 3 Publications Verification Ethylenediaminetetraacetic acid dipotassium dihydrate
EDTA (Ethylenediaminetetraacetic acid) dipotassium dihydrate is anticoagulants, chelating heavy metal and relieve toxicity. EDTA dipotassium dihydrate can damage chromosomes, interfere with the DNA repair process, increase the incidence of meiosis exchange .

HY-Y0958

Methoxyamine hydrochloride O-Methylhydroxylamine hydrochloride
Methoxyamine (O-Methylhydroxylamine) hydrochloride is an orally active and potent *base excision repair* (BER)** inhibitor. Methoxyamine hydrochloride binds to 3’ hydroxyl groups that are left behind by 3-methylpurine-DNA glycosylase (MPG) following excision of the damaged base and thus inhibits BER activity. Methoxyamine hydrochloride binds directly to the apyrimidinic (AP) sites. Methoxyamine hydrochloride synergistically enhances the therapeutic efficacy of DNA-damaging agents .

HY-138155

NSC15520	Others	Cancer
NSC15520 is a small molecular inhibitor of Replication Protein A (RPA). NSC15520 specifically recognizes the RPA N-terminal DNA binding domain (DBD), and blocks the interaction of RPA with p53 or RAD9. NSC15520 also inhibtis helix destabilization of a duplex DNA (dsDNA) oligonucleotide, involves in DNA replication, DNA repair, DNA recombination, and DNA damage response signaling .

HY-13599

Cladribine 3 Publications Verification 2-Chloro-2′-deoxyadenosine; CldAdo; 2CdA	Adenosine Deaminase Apoptosis	Cardiovascular Disease Cancer
Cladribine (2-Chloro-2′-deoxyadenosine), a purine nucleoside analog, is an orally active adenosine deaminase inhibitor. Cladribine functions as an inhibitor of DNA synthesis to block the repair of the damaged DNA. Cladribine can inhibit DNA methylation. Cladribine has anti-lymphoma activity. Cladribine can be used for the research of several hematologic malignancies and multiple sclerosis .

HY-10619B

Niraparib tosylate Maximum Cited Publications 52 Publications Verification MK-4827 tosylate	PARP Apoptosis	Cancer
Niraparib tosylate (MK-4827 tosylate) is a highly potent and orally bioavailable PARP1 and PARP2 inhibitor with an IC₅₀ of 3.8 and 2.1 nM, respectively. Niraparib tosylate leads to inhibition of repair of DNA damage, activates apoptosis and shows anti-tumor activity .

HY-152147

SZUH280	PROTACs HDAC Apoptosis DNA/RNA Synthesis	Cancer
SZUH280 is a potent and selective PROTAC HDAC8 degrader with a DC₅₀ of 0.58 μM in A549 cells. SZUH280 induces cancer cell apoptosis. SZUH280 hampers **DNA damage** repair in cancer cells, promoting cellular radiosensitization .

HY-155038

Antitumor agent-104	PARP CDK	Cancer
Antitumor agent-104 (Compound 9) is an antitumor agent by inhibiting DNA damage repair in tumors. Antitumor agent-104 inhibits PARP1 enzymatic activity and the PAR protein level. Antitumor agent-104 also inhibits the expression of CDK12 .

HY-10619

Niraparib Maximum Cited Publications 52 Publications Verification MK-4827	PARP Apoptosis	Cancer
Niraparib (MK-4827) is a highly potent and orally bioavailable PARP1 and PARP2 inhibitor with IC₅₀s of 3.8 and 2.1 nM, respectively. Niraparib leads to inhibition of repair of DNA damage, activates apoptosis and shows anti-tumor activity .

HY-10619A

Niraparib hydrochloride Maximum Cited Publications 52 Publications Verification MK-4827 hydrochloride	PARP Apoptosis	Cancer
Niraparib hydrochloride (MK-4827 hydrochloride) is a highly potent and orally bioavailable PARP1 and PARP2 inhibitor with IC₅₀s of 3.8 and 2.1 nM, respectively. Niraparib hydrochloride leads to inhibition of repair of DNA damage, activates apoptosis and shows anti-tumor activity .

HY-10619E

Niraparib tosylate hydrate Maximum Cited Publications 52 Publications Verification MK-4827 tosylate hydrate	PARP Apoptosis	Cancer
Niraparib (MK-4827) tosylate hydrate is a highly potent and orally bioavailable PARP1 and PARP2 inhibitor with IC₅₀s of 3.8 and 2.1 nM, respectively. Niraparib tosylate hydrate leads to inhibition of repair of DNA damage, activates apoptosis and shows anti-tumor activity .

HY-138084

SIC5-6	Separase	Cancer
SIC5-6 is a potent Separase inhibitor. Separase, a large cysteine protease, involves in chromosome segregation during mitosis and meiosis, DNA damage repair, centrosome disengagement and duplication, spindle stabilization and elongation. Separase is highly overexpressed in many solid cancers, serves as an attractive chemotherapeutic target .

HY-122198

ML367	Others	Cancer
ML367 is a potent inhibitor of ATPase family AAA domain-containing protein 5 (ATAD5) stabilization, acts as a probe molecule that has low micromolar inhibitory activity. ML367 blocks DNA repair pathways, suppresses general DNA damage responses including RPA32-phosphorylation and CHK1-phosphorylation in response to UV irradiation .

HY-153791

FEN1-IN-6	FLAP	Cancer
FEN1-IN-6 (compound 9) is a potent inhibitor of Flap endonuclease-1 (FEN1, IC₅₀=10 nM), involving in mammalian cells to repair DNA damage. FEN1-IN-6 also targets to related endonuclease, xeroderma pigmentosum G (XPG) with an IC₅₀ value of 23 nM .

HY-150147

CAM833	RAD51 Apoptosis	Cancer
CAM833 is a potent orthosteric inhibitor of the interaction between BRCA2 and RAD51 with a K_d of 366 nM against the ChimRAD51 protein. CAM833 also inhibits RAD51 oligomerization. CAM833 increases the progression of G2/M-arrested cells into apoptosis .

HY-W177546

CD00509	Phosphodiesterase (PDE)	Cancer
CD00509 is a Tdp1 inhibitor, with an IC₅₀ value of 0.71 μM. CD00509 can sensitize breast cancer cells to Camptothecin (HY-16560). CD00509 has anti-tumor activity .

HY-153792

FEN1-IN-7	FLAP	Cancer
FEN1-IN-7 (compound 16) is a selective inhibitor of Flap endonuclease-1 (FEN1, IC₅₀=18 nM), involving in mammalian cells to repair DNA damage. FEN1-IN-7 also targets to related endonuclease, xeroderma pigmentosum G (XPG) with an IC₅₀ value of 3.04 μM. FEN1-IN-7 increases the cellular sensitivity of cancer cells to potent DNA alkylating agents or methylating agents .

HY-137316

Phosphoramide mustard	DNA Alkylator/Crosslinker Drug Metabolite	Cancer
Phosphoramide mustard is a biologically active metabolite of Cyclophosphamide (HY-17420), with anticancer activitiy. Phosphoramide mustard induces DNA damage .

HY-137316A

Phosphoramide mustard cyclohexanamine 1 Publications Verification	DNA Alkylator/Crosslinker Drug Metabolite	Cancer
Phosphoramide mustard cyclohexanamine is a biologically active metabolite of Cyclophosphamide (HY-17420), with anticancer activitiy. Phosphoramide mustard cyclohexanamine induces DNA damage .

HY-101566A

Elimusertib hydrochloride 5+ Cited Publications BAY 1895344 hydrochloride	ATM/ATR	Cancer
Elimusertib (BAY 1895344) hydrochloride is a potent, orally active and selective ATR inhibitor with an IC₅₀ of 7 nM. Elimusertib hydrochloride has anti-tumor activity . Elimusertib hydrochloride can be used for the research of solid tumors and lymphomas .

HY-101566

Elimusertib 5+ Cited Publications BAY 1895344	ATM/ATR	Cancer
Elimusertib (BAY-1895344) is a potent, orally active and selective ATR inhibitor with an IC₅₀ of 7 nM. Elimusertib has anti-tumor activity . Elimusertib can be used for the research of solid tumors and lymphomas .

HY-149398

PARP-1/2-IN-2	Apoptosis PARP CDK	Cancer
PARP-1/2-IN-2-IN-1 (Compound 12e) is a PARP1/2/CDK12 inhibitor (IC₅₀: 34, 30 and 285 nM respectively). PARP-1/2-IN-2 inhibits DNA damage repair, promotes cell cycle arrest and apoptosis. PARP-1/2-IN-2 inhibits the growth of TNBC cells and TNBC xenograft tumor .

HY-115531

UNC-2170	Others	Cancer
UNC-2170 is a functionally active, fragment-like ligand for 53BP1 (IC₅₀=29 µM; K_d=22 µM). UNC-2170 shows at least 17-fold selectivity for 53BP1 as compared to nine other methyl-lysine (Kme) reader proteins. 53BP1 is a Kme binding protein that plays a central role in DNA Damage Repair (DDR) pathways and is recruited to sites of double-strand breaks (DSB) .

HY-156027

SIRT6-IN-3	Sirtuin HDAC Akt mTOR Ribosomal S6 Kinase (RSK) ERK	Neurological Disease Inflammation/Immunology Endocrinology Cancer
SIRT6-IN-3 (compound 8a) is a selective inhibitor of SIRT6 (IC₅₀=7.49 μM). SIRT6-IN-3 inhibits pancreatic ductal adenocarcinoma (PDAC) cells proliferation and induces apoptosis. SIRT6-IN-3 increases the sensitivity of cancer cells to gemcitabine (HY-17026) via blocking the DNA damage repair pathway. SIRT6-IN-3 is used in pancreatic cancer research .

HY-155965

VEGFR/PARP-IN-1	VEGFR PARP Apoptosis	Cancer
VEGFR/PARP-IN-1 (Compound 14b) is a VEGFR/PARP dual inhibitor (IC₅₀s: 191 nM and 60.9 nM respectively). VEGFR/PARP-IN-1 inhibits DNA damage repair, induces cell apoptosis, and arrests cell in the G2/M phase. VEGFR/PARP-IN-1 has good antiproliferative efficacy against BRCA wild-type breast cancer cells (IC₅₀: 4.1 and 3.5 μM for MDA-MB-231 and MCF-7 cells). VEGFR/PARP-IN-1 is an antitumor and anti-metastasis agent .

HY-144338

PARP1/BRD4-IN-1	Epigenetic Reader Domain PARP Apoptosis DNA/RNA Synthesis	Cancer
PARP1/BRD4-IN-1 is a potent and high selective PARP1/BRD4 inhibitor (IC₅₀s of 49 and 202 nM in PARP1 and BRD4, respectively). PARP1/BRD4-IN-1 represses the expression and activity of PARP1 and BRD4 to synergistically inhibit the malignant growth of pancreatic cancer cells .

HY-150613

PARP1/BRD4-IN-2	Epigenetic Reader Domain PARP Apoptosis	Cancer
PARP1/BRD4-IN-2 is a potent and selective PARP1 and BRD4 inhibitor with IC₅₀ values of 197 nM and 238 nM, respectively. PARP1/BRD4-IN-2 inhibits DNA damage repair, arrests G0/G1 transition and induces apoptosis. PARP1/BRD4-IN-2 has anti-tumor activity in MDA-MB-468 xenograft mouse model. PARP1/BRD4-IN-2 can be used for researching triple-negative breast cancer (TNBC) .

Cat. No.	Product Name

HY-L004

Cell Cycle/DNA Damage Compound Library	2001 compounds
DNA is prone to numerous forms of damage that can injure cells and impair fitness. Cells have developed an array of mechanisms to repair these injuries. Proliferating cells are especially vulnerable to DNA damage due to the added demands of cellular growth and division. Cell cycle checkpoints represent integral components of DNA repair that coordinate cooperation between the machinery of the cell cycle and several biochemical pathways that respond to damage and restore DNA structure. By delaying progression through the cell cycle, checkpoints provide more time for repair before the critical phases of DNA replication, when the genome is replicated, and of mitosis, when the genome is segregated. Loss or attenuation of checkpoint function may increase spontaneous and induced gene mutations and chromosomal aberrations by reducing the efficiency of DNA repair. MCE owns a unique collection of 2001 cell cycle/DNA damage-related compounds which can be used in the research of the same.

Cell Cycle/DNA Damage Compound Library

2001 compounds

DNA is prone to numerous forms of damage that can injure cells and impair fitness. Cells have developed an array of mechanisms to repair these injuries. Proliferating cells are especially vulnerable to DNA damage due to the added demands of cellular growth and division. Cell cycle checkpoints represent integral components of DNA repair that coordinate cooperation between the machinery of the cell cycle and several biochemical pathways that respond to damage and restore DNA structure. By delaying progression through the cell cycle, checkpoints provide more time for repair before the critical phases of DNA replication, when the genome is replicated, and of mitosis, when the genome is segregated. Loss or attenuation of checkpoint function may increase spontaneous and induced gene mutations and chromosomal aberrations by reducing the efficiency of DNA repair.

MCE owns a unique collection of 2001 cell cycle/DNA damage-related compounds which can be used in the research of the same.

HY-L179

Radiosensitizer Library	41 Compounds compounds
Radiotherapy is a common treatment for various cancers, and more than 50% of cancer patients require radiotherapy during the disease treatment. With advances in radiation technology and a better understanding of tumor biology, the efficacy of radiation therapy has gradually improved, and more and more patients have benefited from it. However, even with the use of advanced radiotherapy techniques, there are still many malignant tumor cells with low sensitivity to radiation, leading to the radiation effect is not ideal. To solve this problem, radiosensitizers have received more and more attention. Radiosensitizer is a kind of drug that can enhance the radiosensitivity of tumor cells and improve the effect of radiotherapy. Radiation sensitizers act in a variety of ways, such as killing hypoxic cells, enhancing DNA damage, inhibiting DNA damage repair, and blocking cell cycle progression, making tumor cells more susceptible to radiation damage and death than surrounding normal cells. MCE designs a unique collection of 41 compounds with definite reported radiosensitization. It can be used for drug combination research in anti-cancer treatment.

Radiosensitizer Library

41 Compounds compounds

Radiotherapy is a common treatment for various cancers, and more than 50% of cancer patients require radiotherapy during the disease treatment. With advances in radiation technology and a better understanding of tumor biology, the efficacy of radiation therapy has gradually improved, and more and more patients have benefited from it. However, even with the use of advanced radiotherapy techniques, there are still many malignant tumor cells with low sensitivity to radiation, leading to the radiation effect is not ideal. To solve this problem, radiosensitizers have received more and more attention. Radiosensitizer is a kind of drug that can enhance the radiosensitivity of tumor cells and improve the effect of radiotherapy. Radiation sensitizers act in a variety of ways, such as killing hypoxic cells, enhancing DNA damage, inhibiting DNA damage repair, and blocking cell cycle progression, making tumor cells more susceptible to radiation damage and death than surrounding normal cells.

MCE designs a unique collection of 41 compounds with definite reported radiosensitization. It can be used for drug combination research in anti-cancer treatment.

HY-L024

Histone Modification Research Compound Library

614 compounds

A histone modification, a covalent post-translational modification (PTM) to histone proteins, includes methylation, phosphorylation, acetylation, ubiquitylation, and sumoylation, etc. In general, histone modifications are catalyzed by specific enzymes that act predominantly at the histone N-terminal tails involving amino acids such as lysine or arginine, as well as serine, threonine, tyrosine, etc. The PTMs made to histones can impact gene expression by altering chromatin structure or recruiting histone modifiers. Histone modifications act in diverse biological processes such as transcriptional activation/inactivation, chromosome packaging, and DNA damage/repair. Deregulation of histone modification contributes to many diseases, including cancer and autoimmune diseases.

MCE owns a unique collection of 614 bioactive compounds targeting Epigenetic Reader Domain, HDAC, Histone Acetyltransferase, Histone Demethylase, Histone Methyltransferase, Sirtuin, etc. Histone Modification Research Compound Library is a useful tool for histone modification research and drug screening.

HY-L135

Cancer Stem Cells Compound Library

2116 compounds

With the progress of modern cancer therapy, the life of cancer patients has been extended. However, after initial treatment and recovery, the development of secondary tumors often leads to cancer recurrence. Cancer stem cells are a small number of cells that tumor growth and reproduction depend on.

Cancer stem cells have strong self-renewal ability, which is the direct cause of tumor occurrence. In addition, cancer stem cells also have the ability to differentiate into different cell types, playing a crucial role in tumor metastasis and development. Chemotherapy and radiotherapy induced DNA damage and apoptosis are common cancer treatments. However, cancer stem cells can effectively protect cancer cells from apoptosis by activating DNA repair ability. Cancer stem cells are regarded as the key "seed" of tumor occurrence, development, metastasis and recurrence. Since its first discovery in leukemia in 1994, cancer stem cells have been considered a promising therapeutic target for cancer treatment.

MCE supplies a unique collection of 2116 compounds targeting key proteins in cancer stem cells. MCE Cancer Stem Cells Compound Library is a useful tool for cancer stem cells related research and anti-cancer drug development.

HY-L050

Ubiquitination Compound Library

286 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 286 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.

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