MK-4827 |
Catalog No.GC17802
One-Click Copy Product Info
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MK-4827 is an orally active PARP inhibitor that simultaneously inhibits both PARP1 (IC50=3.8nM) and PARP2 (IC50=2.1nM). MK-4827 blocks DNA repair by inhibiting PARP enzyme activity, thereby inducing cancer cell death.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1038915-60-4
Sample solution is provided at 25 µL, 10mM.
MK-4827 is an orally active PARP inhibitor that simultaneously inhibits both PARP1 (IC50=3.8nM) and PARP2 (IC50=2.1nM). MK-4827 blocks DNA repair by inhibiting PARP enzyme activity, thereby inducing cancer cell death[1-2]. MK-4827 is used in research for the treatment of various types of cancer[3-4].
In vitro, treatment of ovarian cancer OVCAR8 cells and pancreatic cancer MIA PaCa-2 cells with MK-4827 (10-20μM) for 48 to 72 hours, MK-4827 significantly suppressed STAT3 phosphorylation, induced apoptosis, downregulated the expression of the anti-apoptotic gene BCL2L1, and upregulated the expression of the pro-apoptotic genes CASP3, CASP8, and CASP9[5]. In esophageal squamous cell carcinoma KYSE-30 and KYSE-150 cells, treatment with MK-4827 (5μM) combined with radiotherapy (4Gy) for 24 hours, MK-4827 markedly enhanced radiation-induced DNA double-strand break damage (increased γ-H2AX expression) and promoted apoptosis, while also increasing radiosensitivity by inhibiting FANCG expression[6].
In vivo, in an ovarian cancer peritoneal metastasis model, oral administration of MK-4827 (50mg/kg) to tumor-bearing mice (inoculated with ID8 cells or patient-derived xenografts) three times per week for 3-8 weeks, starting from day 3 or 6 post-inoculation, MK-4827 significantly inhibited tumor growth, reduced the number of abdominal lesions and ascites volume, and induced ferroptosis in tumor cells[7]. In an atherosclerosis model, oral administration of MK-4827 (10mg/kg) to high-fat diet-fed ApoE⁻/⁻ or Ldlr⁻/⁻ mice three times per week for 8-12 weeks, starting from week 4 or 16 of dietary intervention, MK-4827 significantly reduced atherosclerotic plaque burden, decreased necrotic core area, increased fibrous cap thickness, and suppressed phenotypic switching of smooth muscle cells[8].
References:
[1] Jones P, Altamura S, Boueres J, et al. Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors. J Med Chem. 2009 Nov 26;52(22):7170-85.
[2] Bridges KA, Toniatti C, Buser CA, et al. Niraparib (MK-4827), a novel poly(ADP-Ribose) polymerase inhibitor, radiosensitizes human lung and breast cancer cells. Oncotarget. 2014 Jul 15;5(13):5076-86.
[3] Wang L, Mason KA, Ang KK, et al. MK-4827, a PARP-1/-2 inhibitor, strongly enhances response of human lung and breast cancer xenografts to radiation. Invest New Drugs. 2012 Dec;30(6):2113-20.
[4] Mirza MR, Monk BJ, Herrstedt J, et al. Niraparib Maintenance Therapy in Platinum-Sensitive, Recurrent Ovarian Cancer. N Engl J Med. 2016 Dec 1;375(22):2154-2164.
[5] Zhao Q, Kohut A, Li YJ, et al. Niraparib-induced STAT3 inhibition increases its antitumor effects. Front Oncol. 2022 Oct 17;12:966492.
[6] Cui Y, Huang W, Du F, et al. Therapeutic benefits of niraparib tosylate as radio sensitizer in esophageal squamous cell carcinoma: an in vivo and in vitro preclinical study. Clin Transl Oncol. 2022 Aug;24(8):1643-1656.
[7] Jin N, Qian YY, Jiao XF, et al. Niraparib restricts intraperitoneal metastases of ovarian cancer by eliciting CD36-dependent ferroptosis. Redox Biol. 2025 Mar;80:103528.
[8] Pan H, Ho SE, Xue C, et al. Atherosclerosis Is a Smooth Muscle Cell-Driven Tumor-Like Disease. Circulation. 2024 Jun 11;149(24):1885-1898.
| Cell experiment [1]: | |
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Cell lines |
OVCAR8 (human ovarian cancer cell line), MIA PaCa-2 (human pancreatic ductal adenocarcinoma cell line), PANC-1 (human pancreatic ductal adenocarcinoma cell line), PEO1 (human ovarian cancer cell line) |
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Preparation Method |
Cells were maintained in DMEM or RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) at 37°C, 5% CO₂. Cells were treated with MK-4827 at concentrations of 10µM or 20µM for 24 to 72 hours. |
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Reaction Conditions |
10–20μM; 24–72 hours |
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Applications |
MK-4827 significantly inhibited STAT3 phosphorylation (pSTAT3-Y705) in ovarian and pancreatic cancer cell lines, regardless of BRCA mutation status. MK-4827 downregulated the expression of the anti-apoptotic gene BCL2L1 and upregulated pro-apoptotic genes CASP3, CASP8, and CASP9. MK-4827 treatment for 72 hours induced significant apoptosis. The pro-apoptotic effects were mediated through inhibition of the SRC/STAT3 signaling pathway. |
| Animal experiment [2]: | |
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Animal models |
BALB/c nude mice, C57BL/6 mice |
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Preparation Method |
ID8 ovarian cancer cells were injected intraperitoneally into mice. Mice were treated with MK-4827 at 50mg/kg via oral gavage three times per week for 3-8 weeks, either starting from day 6 post-inoculation (prevention) or after 16 weeks of tumor establishment (therapy). |
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Dosage form |
50mg/kg; p.o.; Three times per week for 3-8 weeks. |
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Applications |
MK-4827 significantly inhibited ovarian cancer progression and induced regression of established metastases in mouse models. MK-4827 reduced tumor burden, decreased ascites volume, and diminished the number of abdominal lesions. |
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References: |
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| Cas No. | 1038915-60-4 | SDF | |
| Chemical Name | 2-[4-[(3S)-piperidin-3-yl]phenyl]indazole-7-carboxamide | ||
| Canonical SMILES | C1CC(CNC1)C2=CC=C(C=C2)N3C=C4C=CC=C(C4=N3)C(=O)N | ||
| Formula | C19H20N4O | M.Wt | 320.39 |
| Solubility | ≥ 32 mg/mL in DMSO, ≥ 50.9 mg/mL in EtOH with gentle warming | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.1212 mL | 15.606 mL | 31.212 mL |
| 5 mM | 624.2 μL | 3.1212 mL | 6.2424 mL |
| 10 mM | 312.1 μL | 1.5606 mL | 3.1212 mL |
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Quality Control & SDS
- View current batch:
- Purity: >98.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)