Product Name :
CNDAC
Description:
CNDAC is a major metabolite of oral drug sapacitabine, and a nucleoside analog.
CAS:
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
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.
Additional information:
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.{{Kaempferol} web|{Kaempferol} Apoptosis|{Kaempferol} Purity & Documentation|{Kaempferol} Data Sheet|{Kaempferol} custom synthesis|{Kaempferol} Autophagy} Deficiency in two Rad51 paralogs, Rad51D and XRCC3, greatly sensitize cells to CNDAC.{{Pertuzumab (anti-HER2)} web|{Pertuzumab (anti-HER2)} Inhibitor|{Pertuzumab (anti-HER2)} TGF-beta/Smad|{Pertuzumab (anti-HER2)} Technical Information|{Pertuzumab (anti-HER2)} Purity|{Pertuzumab (anti-HER2)} manufacturer} The Rad51D-null cell line is approximately 50-fold more sensitive to CNDAC (IC50=0.PMID:25804060 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.|