1. MAPK/ERK Pathway
  2. JNK

Bentamapimod (Synonyms: AS 602801)

Cat. No.: HY-14761 Purity: 98.66%
Handling Instructions

Bentamapimod (AS 602801) is an ATP-competitive JNK inhibitor with IC50 of 80 nM, 90 nM, and 230 nM for JNK1, JNK2, and JNK3, respectively.

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

Bentamapimod Chemical Structure

Bentamapimod Chemical Structure

CAS No. : 848344-36-5

Size Price Stock Quantity
10 mM * 1 mL in DMSO USD 296 In-stock
Estimated Time of Arrival: December 31
5 mg USD 269 In-stock
Estimated Time of Arrival: December 31
10 mg USD 432 In-stock
Estimated Time of Arrival: December 31
50 mg USD 1728 In-stock
Estimated Time of Arrival: December 31
100 mg   Get quote  
200 mg   Get quote  

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    Bentamapimod purchased from MCE. Usage Cited in: Oncotarget. 2016 May 10;7(19):27021-32.

    AS602801 treatment causes loss of stem cell marker expression in cancer stem cells. Subsequent analysis revealed that the levels of other stem cell markers, such as Sox2, Nanog, and Bmi1, are decreased similarly to CD133.

    Bentamapimod purchased from MCE. Usage Cited in: Anticancer Res 38: 6699-6706 (2018)

    Western analysis of Survivin protein expression in the treatment of different concentrations of AS602081 and Carboplatin.

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    • Biological Activity

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    • References


    Bentamapimod (AS 602801) is an ATP-competitive JNK inhibitor with IC50 of 80 nM, 90 nM, and 230 nM for JNK1, JNK2, and JNK3, respectively.

    IC50 & Target


    80 nM (IC50)


    90 nM (IC50)


    230 nM (IC50)

    In Vitro

    Bentamapimod (AS 602801) treatment induces cell death and accordingly decreased the number of viable cells in all three cell lines in a dose-dependent manner, suggesting that Bentamapimod (AS 602801) may have selective cytotoxic activity against neoplastic cells. Bentamapimod (AS 602801) exhibits cytotoxicity against both serum-cultured non-stem cancer cells and cancer stem cells derived from human pancreatic cancer, non-small cell lung cancer, ovarian cancer and glioblastoma at concentrations that did not decrease the viability of normal human fibroblasts. Bentamapimod (AS 602801) also inhibits the self-renewal and tumor-initiating capacity of cancer stem cells surviving Bentamapimod (AS 602801) treatment[2].

    In Vivo

    Treatment of nude mice bearing xenografts biopsied from women with endometriosis (BWE) with 30 mg/kg Bentamapimod (AS 602801) causes 29% regression of lesion. Medroxyprogesterone acetate (MPA) or progesterone (PR) alone did not cause regression of BWE lesions, but combining 10 mg/kg Bentamapimod (AS 602801) with MPA caused 38% lesion regression. In human endometrial organ cultures (from healthy women), treatment with Bentamapimod (AS 602801) or MPA reduced matrix metalloproteinase-3 (MMP-3) release into culture medium. In organ cultures established with BWE, PR or MPA failed to inhibit MMP-3 secretion, whereas AS 602801 alone or MPA + Bentamapimod (AS 602801) suppresses MMP-3 production. In an autologous rat endometriosis model, AS 602801 causes 48% regression of lesions compared to GnRH antagonist Antide (84%). Bentamapimod (AS 602801) reduces inflammatory cytokines in endometriotic lesions, while levels of cytokines in ipsilateral horns are unaffected. Furthermore, Bentamapimod (AS 602801) enhances natural killer cell activity, without apparent negative effects on uterus[3].

    Solvent & Solubility
    In Vitro: 

    10 mM in DMSO

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.1856 mL 10.9278 mL 21.8555 mL
    5 mM 0.4371 mL 2.1856 mL 4.3711 mL
    10 mM 0.2186 mL 1.0928 mL 2.1856 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      AS 602801 stock solution (10 mM in DMSO) is diluted in PBS to prepare 200 μL solutions[2].

    Cell Assay

    PANC-1, A2780, and A549 human cancer cells and IMR90 human normal fibroblasts are treated without (control) or with the indicated concentrations of Bentamapimod (AS 602801) (2.5, 5, and 7.5 μM) for 3 days. The number of viable cells (left panels) and the percentage of dead cells (right panels) are determined using trypan blue as a vital dye[2].

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

    Animal Administration

    The 5-week-old athymic (ncr/nude) ovariectomized mice are anesthetized with isoflurane and subcutaneously implanted with a silastic capsule containing 8 μg estradiol. Twenty-four hours later, mice received subcutaneous or intraperitoneal injection with a phosphate-buffered saline (PBS) suspension of 8 to 10 human endometrial tissue fragments/mouse (biopsies obtained from volunteers or patients) on the ventral midline just below the umbilicus. For 24 hours immediately preceding injection, tissue fragments are established as organ cultures treated with 1 nM estradiol, PR, or MPA. Oral administration of Bentamapimod (AS 602801) is initiated 10 to 12 days following the injection of tissue. Progesterone is provided via a slow-release silastic capsule containing 25 μg PR, and MPA is given by twice-weekly injections (200 mg/kg) along the right flank using a tuberculin syringe. Bentamapimod (AS 602801) is administered by gavage at a dose of 10 mg/kg and 30 mg/kg/animal for 30 days. Following the completion of treatment, mice are again anesthetized and sacrificed by cervical dislocation for direct examination of lesion size and number. Uteri are measured and weighed, and excised lesions rapidly frozen for further analysis[3].

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

    Molecular Weight




    CAS No.




    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month

    Room temperature in continental US; may vary elsewhere

    Purity: 98.66%

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    Cat. No.: HY-14761