The molecular weight of this compound is 540.70 Daltons. This product is tested for solubility in DMSO. The minimum solubility specification is 25 mg/mL. A review of past lots reveals rates ranging from 40 - 46 mg/ml in DMSO. Please see the link below to access a sample or lot-specific Certificate of Analysis:
https://www.sigmaaldrich.com/product/sigma/sml1175#product-documentation
SML1175
Romidepsin
≥98% (HPLC), powder, histone deacetylase inhibitor
Synonyme(s) :
Cyclo[(2Z)-2-amino-2-butenoyl-L-valyl-(3S,4E)-3-hydroxy-7-mercapto-4-heptenoyl-D-valyl-D-cysteinyl] cyclic (35)-disulfide, Depsipeptide, FK228, FR901228, L-Valine, N-((3S,4E)-3-hydroxy-7-mercapto-1-oxo-4-heptenyl)-D-valyl-D-cysteinyl-(2Z)-2-amino-2-butenoxyl-, (4-1)-lactone, cyclic (1-2)-disulfide
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1 MG
352.00 CHF
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1 MG
352.00 CHF
About This Item
Formule empirique (notation de Hill):
C24H36N4O6S2
Numéro CAS:
Poids moléculaire :
540.70
Numéro MDL:
Code UNSPSC :
12352200
ID de substance PubChem :
Nomenclature NACRES :
NA.77
Produits recommandés
Nom du produit
Romidepsin, ≥98% (HPLC)
Niveau de qualité
Essai
≥98% (HPLC)
Forme
powder
Couleur
white to beige
Solubilité
DMSO: 25 mg/mL, clear
Température de stockage
−20°C
Chaîne SMILES
O=C(N/C(C(N[C@@H](C(C)C)C(O[C@@]1([H])CC2=O)=O)=O)=C\C)[C@@H](CSSCC/C=C/1)NC([C@H](N2)C(C)C)=O
InChI
1S/C24H36N4O6S2/c1-6-16-21(30)28-20(14(4)5)24(33)34-15-9-7-8-10-35-36-12-17(22(31)25-16)26-23(32)19(13(2)3)27-18(29)11-15/h6-7,9,13-15,17,19-20H,8,10-12H2,1-5H3,(H,25,31)(H,26,32)(H,27,29)(H,28,30)/b9-7+,16-6-/t15-,17-,19-,20+/m1/s1
Clé InChI
OHRURASPPZQGQM-GCCNXGTGSA-N
Informations sur le gène
human ... HDAC1(3065) , HDAC10(83933) , HDAC11(79885) , HDAC2(3066) , HDAC3(8841) , HDAC4(9759) , HDAC5(10014) , HDAC6(10013) , HDAC7(51564) , HDAC8(55869) , HDAC9(9734)
Actions biochimiques/physiologiques
Romidepsin is a very potent natural prodrug inhibitor of HDAC1 and HDAC2 that is converted to active form by glutathione. Romidepsin has IC50 values of 36 nM and 47 nM for HDAC1 and HDAC2, respectively. Romidepsin kills lymphoma cell lines overexpressing Bcl-2 and Bcl-XL, and has been approved for the treatment for cutaneous T-cell lymphoma (CTCL) and peripheral T-cell lymphoma, and a variety of other cancers.
Romidepsin is a very potent natural prodrug inhibitor of HDAC1 and HDAC2; antineoplastic.
Romidepsin promotes apoptosis, while hindering tumor growth in glioma models.[1]
Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 3
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
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Certificats d'analyse (COA)
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Les clients ont également consulté
Anna Otte et al.
International journal of oncology, 49(6), 2453-2463 (2016-10-18)
Chemotherapeutic drug testing of SCCOHT-1 and BIN-67 tumor cells revealed synergistic growth-inhibition of >95% in vitro with a combination of foretinib and FK228. Application of this drug combination in vivo in NODscid mice-induced SCCOHT-1GFP tumors was associated with ~6-fold reduction in
Sina Jostes et al.
Journal of cellular and molecular medicine, 21(7), 1300-1314 (2016-12-28)
Type II testicular germ cell cancers (TGCT) are the most frequently diagnosed tumours in young men (20-40 years) and are classified as seminoma or non-seminoma. TGCTs are commonly treated by orchiectomy and chemo- or radiotherapy. However, a subset of metastatic
A phase I/II trial of the histone deacetylase inhibitor romidepsin for adults with recurrent malignant glioma: North American Brain Tumor Consortium Study 03-03.
Iwamoto F M, et al.
Neuro-Oncology, 13(5), 509-516 (2011)
Sara Moron-Lopez et al.
AIDS (London, England), 33(3), 425-431 (2018-12-12)
Reversing HIV-1 latency has been suggested as a strategy to eradicate HIV-1. We investigated the effect of romidepsin on the HIV transcription profile in participants from the REDUC part B clinical trial. Seventeen participants on suppressive antiretroviral therapy were vaccinated
Minsun Jung et al.
The oncologist, 24(8), e740-e748 (2019-01-31)
NUT carcinoma is a rare aggressive disease caused by BRD4/3-NUT fusion, and C-MYC upregulation plays a key role in the pathogenesis. Here, we report on the clinicopathological characteristics of Korean patients with NUT carcinoma and the in vitro efficacy of
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