A Na+/K+-ATPase inhibitor
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Resibufogenin

Item No. 9001348

Technical Information
Formal Name
(3β,5β,15β)-14,15-epoxy-3-hydroxy-bufa-20,22-dienolide
CAS Number
465-39-4
Synonyms
  • Bufogenin
  • NSC 90783
  • Respigon
Molecular Formula
C24H32O4
Formula Weight
Purity
≥98%
Formulation
A crystalline solid
DMF: 25 mg/mLDMF:PBS(pH 7.2)(1:1): 0.5 mg/mLDMSO: 20 mg/mLEthanol: 5 mg/mL
λmax
299 nm
SMILES
O=C(C=C1)OC=C1[C@H]2C[C@@H]3[C@]4(O3)[C@]5([H])CC[C@]6([H])C[C@@H](O)CC[C@]6(C)[C@@]5([H])CC[C@@]42C
InChi Code
InChI=1S/C24H32O4/c1-22-9-7-16(25)11-15(22)4-5-18-17(22)8-10-23(2)19(12-20-24(18,23)28-20)14-3-6-21(26)27-13-14/h3,6,13,15-20,25H,4-5,7-12H2,1-2H3/t15-,16+,17+,18-,19-,20-,22+,23-,24-/m1/s1
InChi Key
ATLJNLYIJOCWJE-CWMZOUAVSA-N
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    Product Description

    Resibufogenin is a cardiac glycoside first isolated from Bufonis venom that acts as an inhibitor of the Na+/K+-ATPase.1 It exhibits cardiotonic, vasopressor, and respiratory stimulating actions in both animal and clinical models.2 Resibufogenin has been used to antagonize the action of marinobufagenin in a rat experimental model of preeclampsia.3 Resibufogenin is also reported to have antiproliferative effects against cancer cells, inducing cell cycle arrest by suppressing the expression of cyclin D1.4

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Pamnani, M.B., Chen, S., Bryant, H.J., et alEffects of three sodium-potassium adenosine triphosphatase inhibitors. Hypertension 18(3), 316-324 (1991).

    2. Iwatsuki, K., Yusa, T., Kataoka, Y., et alExperimental and clinical studies of resibufogenin. Tohoku J. Exp. Med. 86(2), 93-101 (1965).

    3. Puschett, J.B., Agunanne, E., and Uddin, M.N. Marinobufagenin, resibufogenin and preeclampsia. Biochim. Biophys. Acta 1802(12), 1246-1253 (2010).

    4. Ichikawa, M., Sowa, Y., Iizumi, Y., et alResibufogenin induces G1-phase arrest through the proteasomal degradation of cyclin D1 in human malignant tumor cells. PLoS One 10(6), (2015).