CNDAC


Catalog No. Size PriceQuantity
M21444-C Contact sales@xcessbio.com for quotation $100Unavailable

Description

CNDAC is a major metabolite of oral drug sapacitabine, and a nucleoside analog.

Product information

CAS Number: 135598-68-4

Molecular Weight: 252.23

Formula: C10H12N4O4

Chemical Name: (2R,3S,4S,5R)-2-(4-amino-2-oxo-1,2-dihydropyrimidin-1-yl)-4-hydroxy-5-(hydroxymethyl)oxolane-3-carbonitrile

Smiles: NC1C=CN([C@@H]2O[C@H](CO)[C@@H](O)[C@@H]2C#N)C(=O)N=1

InChiKey: DCYBPMFXJCWXNB-JWIUVKOKSA-N

InChi: InChI=1S/C10H12N4O4/c11-3-5-8(16)6(4-15)18-9(5)14-2-1-7(12)13-10(14)17/h1-2,5-6,8-9,15-16H,4H2,(H2,12,13,17)/t5-,6+,8-,9+/m0/s1

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

In Vitro:

CNDAC-induced SSBs can be repaired by the transcription-coupled nucleotide excision repair pathway, whereas lethal DSBs are mainly repaired through homologous recombination. Deficiency in two Rad51 paralogs, Rad51D and XRCC3, greatly sensitize cells to CNDAC. The Rad51D-null cell line is approximately 50-fold more sensitive to CNDAC (IC50=0.006 µM) compared to 51D1.3, the Rad51D-repleted line (IC50=0.32 µM). CNDAC shows inhibitory activity against HL-60 and THP-1 cells with IC50s of 1.58 µM and 0.84 µM. CNDAC (10 μM) results in a significant drop in cell survival compared to the untreated on days 4, 7, and 14. CNDAC is more effective at reducing viability and inducing apoptosis than ara-C at equivalent concentrations in the THP-1 cell line, which is defined as displaying resistance to ara-C. CNDAC induces DSBs, which are products of replication, rather than a consequence of induction of apoptosis. CNDAC causes DNA damage, and DNA-PK and ATR are dispensable for cell survival. CNDAC exhibits potent activity against human fibroblasts deficient in ATM or transfected with an empty vector, approximately 30-fold more than cells repleted with full-length ATM cDNA, with IC50s of 0.01 μM and 0.3 μM, respectively. CNDAC-induced DNA damage is repaired through the homologous recombination pathway.

Products are for research use only. Not for human use.

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