2. Cell Cycle/DNA Damage Apoptosis
  3. DNA Alkylator/Crosslinker Bcl-2 Family Caspase Apoptosis Topoisomerase
  4. MN33-63

MN33-63 is a Bcl-2 inhibitor, caspase-3 activator and DNA crosslinker with broad-spectrum anticancer activity. MN33-63 improves the water solubility of SN-38 (HY-13704), inhibits tumor growth and proliferation in a dose-dependent manner, and causes no obvious toxicity. MN33-63 relieves the inhibition of the mitochondrial apoptotic pathway, initiates the apoptosis program, inhibits Topo I activity, and promotes its degradation via the ubiquitin-proteasome and autophagy-lysosome pathways. MN33-63 induces DNA crosslinking, G2/M cell cycle arrest, inhibition of cancer cell migration, and cancer cell apoptosis through the mitochondrial pathway. MN33-63 can be used in the research of colorectal cancer, cervical cancer, hepatocellular carcinoma, lung adenocarcinoma and gastric cancer.

For research use only. We do not sell to patients.

MN33-63

MN33-63 Chemical Structure

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MN33-63 Related Antibodies

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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Topoisomerase Topo I Topo II DNA gyrase

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Description

MN33-63 is a Bcl-2 inhibitor, caspase-3 activator and DNA crosslinker with broad-spectrum anticancer activity. MN33-63 improves the water solubility of SN-38 (HY-13704), inhibits tumor growth and proliferation in a dose-dependent manner, and causes no obvious toxicity. MN33-63 relieves the inhibition of the mitochondrial apoptotic pathway, initiates the apoptosis program, inhibits Topo I activity, and promotes its degradation via the ubiquitin-proteasome and autophagy-lysosome pathways. MN33-63 induces DNA crosslinking, G2/M cell cycle arrest, inhibition of cancer cell migration, and cancer cell apoptosis through the mitochondrial pathway. MN33-63 can be used in the research of colorectal cancer, cervical cancer, hepatocellular carcinoma, lung adenocarcinoma and gastric cancer[1].

IC50 & Target

Caspase 3

 

Bcl-2

 

Topoisomerase I

 

In Vitro

MN33-63 potently inhibits the proliferation of HCT-15, HeLa, HepG2, A549, HGC-27 and CT26 cancer cells, with an IC50 range of 0.05 nM-306.10 nM at 72 h, and exhibits the strongest activity against HGC-27 cells[1].
MN33-63 (100 nM; 24-48 h) potently inhibits the migration of CT26 cells, resulting in a migration rate of 2.51% at 24 h and 4.42% at 48 h[1].
MN33-63 (100 nM; 48 h) induces strong G2/M phase arrest in CT26 cells, with 59.8% of cells residing in the G2/M phase after 48 h of incubation[1].
MN33-63 (100 nM; 48 h) induces apoptosis in 61.10% of CT26 cells, and after 48 h of incubation, its pro-apoptotic activity is stronger than that of chlormethine hydrochloride (HY-B1253) (CH), SN-38 (HY-13704), or their physical mixture[1].
MN33-63 (1-10000 nM, 1 μM; 72 h) reduces Topo I protein levels in CT26 cells in a dose-dependent manner within 72 h. Its inhibitory effect is significant at the concentration of 1 μM, and is superior to that of SN-38, CH and their physical mixture[1].
MN33-63 (1 μM; 72 h) downregulates Bcl-2 expression and reduces the total caspase-3 protein level in CT26 cells, thereby activating the intrinsic apoptotic pathway[1].
MN33-63 (1 μM + 2 μM MG132 (HY-13259); 1 μM + 50 μM chloroquine; 72 h) promotes the degradation of Topo I in CT26 cells via both the ubiquitin-proteasome and autophagy-lysosome pathways; after 72 h of incubation, MG132 and chloroquine reverse the reduction of Topo I[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

MN33-63 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: HCT-15, HeLa, HepG2, A549, HGC-27, CT26
Concentration: 0.038-100000 nM
Incubation Time: 72 h
Result: Exhibited broad-spectrum antiproliferative activity across all six cell lines, with IC50 values of 49.07 nM (HCT-15), 22.94 nM (HeLa), 9.47 nM (HepG2), 306.10 nM (A549), 0.05 nM (HGC-27), and 9.78 nM (CT26).
Showed superior potency to SN-38, CH, and their physical mixture in most cell lines, particularly exceptional activity against HGC-27 cells.

Western Blot Analysis[1]

Cell Line: CT26
Concentration: 1-10000 nM, 1 μM
Incubation Time: 72 h
Result: Reduced Topo I protein levels in a dose-dependent manner, with significant inhibition observed at concentrations as low as 1 μM.
At 1 μM, inhibited Topo I expression more effectively than SN-38, CH, or their physical mixture.

Western Blot Analysis[1]

Cell Line: CT26
Concentration: 1 μM
Incubation Time: 72 h
Result: Significantly downregulated Bcl-2 expression and reduced total caspase-3 protein levels (reflecting activation and cleavage of pro-caspase-3) compared to SN-38, CH, or their physical mixture.

Western Blot Analysis[1]

Cell Line: CT26
Concentration: 1 μM MN33-63 + 2 μM MG132; 1 μM MN33-63 + 50 μM CQ
Incubation Time: 72 h
Result: The reduction in Topo I protein levels induced by MN33-63 was significantly reversed by both MG132 and CQ, indicating MN33-63 promotes Topo I degradation via the ubiquitin-proteasome and autophagy-lysosome pathways.
In Vivo

MN33-63 (1.79-7.16 mg/kg; i.p.; daily; 10 days) exhibits dose-dependent, potent antitumor activity in CT26 tumor-bearing BALB/c mice, with a high-dose tumor weight inhibition rate of 77.10%, and maintains a favorable safety profile with no observed organ toxicity or body weight loss[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c mice with Colorectal cancer (female, 4-5 weeks old, 19-21 g, subcutaneous xenograft model)[1]
Dosage: 1.79 mg/kg; 3.58 mg/kg; 7.16 mg/kg
Administration: i.p.; daily; 10 days
Result: Achieved a tumor weight inhibition rate of 77.10% at 7.16 mg/kg, significantly higher than CH monotherapy, SN-38 monotherapy, and CH + SN-38 physical mixture.
Drastically reduced tumor volume growth in all dose groups, with the 7.16 mg/kg group showing the smallest final tumor volumes.
Caused no body weight loss in any dose group.
Maintained serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine (CREA) levels within normal reference ranges in all dose groups.
Induced dose-dependent increases in tumor tissue necrotic areas, nuclear condensation, and cell apoptosis, with the 7.16 mg/kg group exhibiting the most extensive tumor cell damage.
Showed no abnormal pathological changes (inflammation, necrosis, degeneration) in heart, liver, spleen, lung, and kidney tissues in any dose group.
Molecular Weight

684.37

Formula

C27H26Cl2N3Na2O9P
SMILES

CCC1=C2C(C(N3C2)=CC([C@@](OP(O[Na])(O[Na])=O)(CC)C(OC4)=O)=C4C3=O)=NC5=CC=C(OC(N(CCCl)CCCl)=O)C=C51
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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MN33-63 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

MN33-63DNA Alkylator/CrosslinkerBcl-2 FamilyCaspaseApoptosisTopoisomeraseTopo Imitochondrial apoptosis pathwayBcl-2hepatocellular carcinomacervical cancerlung adenocarcinomacaspase-3ubiquitin-proteasome pathwayautophagy-lysosome pathwaycolorectal cancerInhibitorinhibitorinhibit

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