2. Apoptosis
  3. Apoptosis
  4. Antitumor agent-96

Antitumor agent-96 (Compound D34) is a potent MRE11 inhibitor. Antitumor agent-96 down-regulates the HR pathway by binding with MRE11 and suppressing its endonuclease functions. Antitumor agent-96 induces CM cells apoptosis.

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Antitumor agent-96 Chemical Structure

Antitumor agent-96 Chemical Structure

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Antitumor agent-96 Related Antibodies

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Description

Antitumor agent-96 (Compound D34) is a potent MRE11 inhibitor. Antitumor agent-96 down-regulates the HR pathway by binding with MRE11 and suppressing its endonuclease functions. Antitumor agent-96 induces CM cells apoptosis[1].

IC50 & Target

MRE11[1]
In Vitro

Antitumor agent-96 (Compound D34; 72 h) has a particular cytotoxicity selectivity in CM cells of CM-AS16 (IC50 = 2.9±0.1 μM), CRMM2 (IC50 = 0.7 ± 0.0 μM), CM2005.1 (IC50 = 1.0 ± 0.1 μM), and CRMM1 (IC50 = 1.3 ± 0.3 μM), compared to ocular melanoma, cutaneous melanoma and normal cells[1].
Antitumor agent-96 (0.1-10 μM; 48 h) induces CRMM1 cell apoptosis[1].
Antitumor agent-96 (0.3 μM; 0-72 h) inhibits CRMM1 cell migration[1].
Antitumor agent-96 (0.3-10 μM; 48 h) augments DNA damage accumulation in CM cells and down-regulates MRN complex in HR pathway[1].

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

Antitumor agent-96 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: CM-AS16, CRMM2 , CM2005.1, CRMM1, HL7702 and PIG1
Concentration:
Incubation Time: 72 h
Result: Inhibited proliferation with IC50s of 2.9 ± 0.1, 0.7 ± 0.0, 1.0 ± 0.1, 1.3 ± 0.3, 25.6 ± 0.8 and 32.9 ± 0.3 μM against CM-AS16, CRMM2, CM2005.1, CRMM1, HL7702 and PIG1, respectively.

Apoptosis Analysis[1]

Cell Line: CRMM1 cells
Concentration: 0.1, 0.3, 1, 3 and 10 μM
Incubation Time: 48 h
Result: Significantly led to CRMM1 cells death over the concentrations of 0.3 μM. The apoptotic rates rose to 80% when incubated at 3 μM.

Cell Migration Assay [1]

Cell Line: CRMM1 cells
Concentration: 0.3 μM
Incubation Time: 0, 24, 48 and 72 h
Result: Inhibited migration rate from 70% to 45% at 72 h.

Western Blot Analysis[1]

Cell Line: CRMM1 and CRMM2
Concentration: 0.3, 1, 3 and 10 μM
Incubation Time: 48 h
Result: Stimulated tumor suppressor p53. Induced significant accumulation of γ-H2AX. The three MRN subunits MRE11, RAD50, and NBS1, were significantly down-regulated in a dose-dependent manner. The expression of MRN downstream effectors, including BCRA1 and RAD51, were also inhibited in both CRMM1 and CRMM2 cells.
In Vivo

Antitumor agent-96 dihydrochloride (Compound D34 dihydrochloride; 10 and 20 mg/kg; i.p.; five times per week for 28 days) shows anti-tumor effect in mice[1].

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

Animal Model: NCG mice, CRMM1 xenograft tumor model[1]
Dosage: 10 mg/kg and 20 mg/kg
Administration: Intraperitoneal injection, five times per week for 28 days
Result: Suppressed tumor growth. Did not induce any conspicuous body weight loss.
Molecular Weight

416.56

Formula

C27H32N2O2
SMILES

O=C(C1=C2C=CC=CC2=CC=C1OCCCN3CCNCC3)CCCC4=CC=CC=C4
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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Antitumor agent-96 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:

Antitumor agent-96Antitumor agent96Antitumor agent 96ApoptosisCM-AS16CRMM2 CM2005.1CRMM1MRE11RAD50NBS1γ-H2AXInhibitorinhibitorinhibit

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