| Stereochemistry | ABSOLUTE |
| Molecular Formula | C9H13N3O4.ClH |
| Molecular Weight | 263.678 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 3 / 3 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
Cl.NC1=NC(=O)N(C=C1)[C@H]2C[C@H](O)[C@@H](CO)O2
InChI
InChIKey=LTKCXZGFJFAPLY-OERIEOFYSA-N
InChI=1S/C9H13N3O4.ClH/c10-7-1-2-12(9(15)11-7)8-3-5(14)6(4-13)16-8;/h1-2,5-6,8,13-14H,3-4H2,(H2,10,11,15);1H/t5-,6+,8+;/m0./s1
| Molecular Formula | ClH |
| Molecular Weight | 36.461 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
| Molecular Formula | C9H13N3O4 |
| Molecular Weight | 227.2172 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 3 / 3 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
2′-Deoxycytidine (deoxyC) is one of the deoxy nucleosides, which after phosphorylation to dCTP is used to synthesize DNA via various DNA polymerases or reverse transcriptases. Deoxycytidine is phosphorylated by deoxycytidine kinase (dCK). This enzyme catalyzes the initial conversion of the nucleosides deoxyadenosine (dA), deoxyguanosine (dG), and deoxycytidine (dC) into their monophosphate forms, with subsequent phosphorylation to the triphosphate forms performed by additional enzymes.
CNS Activity
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
Sample Use Guides
It was examined the effect of supraphysiologic concentrations of the naturally occurring nucleoside deoxycytidine (dCyd) on the in vitro growth of normal (CFU-GM) and leukemic (L-CFU) myeloid progenitor cells. Bone marrow samples obtained from 34 consecutive patients undergoing routine diagnostic bone marrow aspirations for nonmalignant hematologic disorders exhibited nearly a twofold increment in CFU-GM when continuously cultured in the presence of 10(-4) mol/L dCyd. Higher dCyd concentrations were associated with a smaller degree of enhancement of colony formation. In contrast, the growth of leukemic blast progenitors obtained from patients with acute nonlymphocytic leukemia were not enhanced by any of the dCyd concentrations tested. Treatment of normal bone marrow cells with dCyd at concentrations ranging from 10(-6) to 5 X 10(-3) mol/L for 24 hours had only a minor effect on the fraction of CFU-GM in S phase. Coadministration of 10(-4) mol/L dCyd was able to reverse the inhibitory effects of several putative regulators of normal myelopoiesis, including leukemia inhibitory activity (LIA), acidic isoferritins (AIF), and prostaglandin E1 (PGE1). Leukemic myeloblasts exposed to 10(-4) mol/L dCyd exhibited substantial expansion of intracellular pools of dCyd triphosphate (dCTP), demonstrating that inability to metabolize dCyd could not be solely responsible for the absence of growth potentiation in these cells. It was suggested that supraphysiologic concentrations of dCyd might the former from the inhibitory effects of several potential negative regulators of myelopoiesis.
