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Zalcitabine (ddC; Dideoxycytidine)

Alias: ddC; Dideoxycytidine; 2'',3''-Dideoxycytidine; Ro 24-2027/000; Ro-24-2027/000; Ro 24-2027 000; NSC606170; NSC 606170; NSC-606170; Zalcitabine; ddC; zalcitabine; Dideoxycytidine; 7481-89-2; 2',3'-DIDEOXYCYTIDINE; ddCyd; HIVID; Cytidine, 2',3'-dideoxy-; ddC; dideoxycytidine, Hivid.
Cat No.:V1822 Purity: ≥98%
Zalcitabine (trade name Hivid) is a nucleoside analog HIV reverse transcriptase inhibitor (NARTI).
Zalcitabine (ddC; Dideoxycytidine)
Zalcitabine (ddC; Dideoxycytidine) Chemical Structure CAS No.: 7481-89-2
Product category: Reverse Transcriptase
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Zalcitabine (trade name Hivid) is a nucleoside analog HIV reverse transcriptase inhibitor (NARTI). It is an antiviral pyrimidine nucleoside analogue effective against HIV replication. 2′,3′-Dideoxycytidine, when activated to its triphosphate, is incorporated into DNA by HIV-1 RT (HIV-1 reverse transcriptase), causing DNA chain termination and viral replication. Zalcitabine was the third antiretroviral to be approved by the Food and Drug Administration (FDA) for the treatment of HIV/AIDS. It is used as part of a combination regimen. Zalcitabine appears less potent than some other nucleoside RTIs, has an inconvenient three-times daily frequency and is associated with serious adverse events. For these reasons it is now rarely used to treat human immunodeficiency virus (HIV), and it has even been removed from pharmacies entirely in some countries.

Biological Activity I Assay Protocols (From Reference)
Targets
HIV reverse transcriptase
ln Vitro
Zalcitabine is an antiviral drug that is phosphorylated to 2',3'-dideoxycytidine 5'-triphosphate (ddCTP) in both HIV-positive and uninfected cells. Zalcitabine is a dideoxynucleoside. Reverse transcriptase is inhibited and proviral DNA chain elongation is stopped when ddCTP is used at therapeutic dosages to prevent HIV replication[1]. With an IC50 value of 1.23 mM, zelcitabine inhibits the cellular absorption of [3H]-PAH in CHO/hOAT1 cells. Additionally, when hOATI activity in CHO/hOAT1 cells rose, zalcitabine's cellular absorption increased threefold[2].
ln Vivo
Zalcitabine is a dideoxynucleoside antiretroviral agent that is phosphorylated to the active metabolite 2',3'-dideoxycytidine 5'-triphosphate (ddCTP) within both uninfected and HIV-infected cells. At therapeutic concentrations, ddCTP inhibits HIV replication by inhibiting the enzyme reverse transcriptase and terminating elongation of the proviral DNA chain. The results of 3 large pivotal trials comparing zidovudine monotherapy with combination therapy have now clearly established that zalcitabine plus zidovudine combination with an improvement in viral load and CD4+ cell count compared with zidovudine monotherapy. More recently, clinical end-point and surrogate marker data have established the efficacy of zalcitabine in combination with the protease inhibitor saquinavir in zidovudine-experienced patients. Other studies have demonstrated the utility of zalcitabine in combination with ritonavir and the nucleoside analogue lamivudine. Importantly, early use of zalcitabine in the treatment sequence does not appear to limit the therapeutic efficacy of subsequent therapy with other nucleoside analogues such as lamivudine. Peripheral neuropathy is the most frequent dose-limiting adverse effect associated with zalcitabine therapy and is generally reversible on discontinuation of treatment. Stomatitis and mouth ulcers may occur frequently with zalcitabine therapy but tend to resolve with continuing treatment. Haematological toxicity, which is a common adverse effect associated with zidovudine, is reported infrequently with zalcitabine. Overall, combination therapy with zalcitabine plus zidovudine or saquinavir has been shown to have a tolerability profile comparable to that of either agent alone, although treatment with zidovudine plus zalcitabine was associated with a significant increase in the incidence of haematological toxicity compared with zidovudine monotherapy in one study. Therefore, current data suggest that zalcitabine is a useful antiretroviral agent for inclusion as a component of initial double combination therapy with zidovudine or as part of triple combination therapy including zidovudine plus a protease inhibitor in the management of patients with HIV infection[1].
Cell Assay
The present study aimed to investigate the interaction of zalcitabine with human organic anion transporter 1 (hOATI) during renal excretion. Contribution of OAT1 to the renal transport of zalcitabine was examined using the transfected cell lines overexpressing the human organic anion transporter1 (CHO/hOAT1 cells). Zalcitabine exhibited the inhibition effect on the cellular uptake of [3H]-PAH in CHO/hOAT1 cells with an IC50 value of 1.23 mM. Furthermore, the cellular uptake of zalcitabine increased threefold with the enhancement of hOATI activity in CHO/hOAT1 cells, while it was significantly reduced in the presence of OAT1 inhibitors such as ketoprofen, naproxen, PAH and 6-carboxyfluorescein. Those results suggest that hOATI contributes at least in part to the cellular uptake of zalcitabine across the basolateral membrane of proximal tubular cells[2].
Animal Protocol


ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Bioavailability is over 80% following oral administration.
Renal excretion of unchanged drug appears to be the primary route of elimination, accounting for approximately 80% of an intravenous dose and 60% of an orally administered dose within 24 hours after dosing (n=19). Renal clearance exceeds glomerular filtration rate suggesting renal tubular secretion contributes to the elimination of zalcitabine by the kidneys.
0.304 to 0.734 L/kg
285 mL/min [HIV-infected patients receiving 1.5 mg IV infusion for 1 hour]
Zalcitabine is eliminated principally in urine. Approximately 60-70% of an oral dose or 75-80% of an IV dose of the drug is eliminated unchanged in urine within 24 hours; approximately 10% of an orally administered dose is eliminated in feces as unchanged drug and ddU.
Only limited information is available on the pharmacokinetics of zalcitabine in children; however, oral bioavailability of the drug appears to be lower in children than in adults. In a study in children 6 months to 13 years of age with symptomatic HIV infection, oral bioavailability of zalcitabine averaged 54% (range: 29-100%). Following oral administration of 0.03- or 0.04-mg/kg doses of zalcitabine every 6 hours in these children, peak plasma concentrations were 23.1-52.5 or 31.5-63 ng/mL, respectively. Following IV administration over 1 hour of 0.03- or 0.04-mg/kg doses of zalcitabine every 6 hours in these children, peak plasma concentrations were 39.9-44.1 or 79.8-165.9 ng/mL, respectively.
Pregnant rhesus monkeys (Macaca mulatta) that were near term (146 days) received radiolabelled zalcitabine as a bolus dose of 0.6 mg/kg body weight via the radial vein. During a 3 hour sampling of both the mother and the fetus, the fetal:maternal ratio of the integrated area under the curve of plasma concentration-time was 0.32 +/- 0.02, and the fetal tissues were found to contain zalcitabine (0.05-0.8 umol/l equivalents) and zalcitabine monophosphate (0.008-0.09 nmol/g).
About 10% of the drug appears in the feces and approximately 75% is excreted unchanged in the urine, suggesting that renal integrity is important for clearance.
For more Absorption, Distribution and Excretion (Complete) data for ZALCITABINE (9 total), please visit the HSDB record page.
Metabolism / Metabolites
Zalcitabine is not reported to undergo significant hepatic metabolism; it is mainly phosphorylated intracellularly to zalcitabine triphosphate, the active substrate for HIV-reverse transcriptase. The concentration of zalcitabine triphosphate remains low for quantitative detection and measurement in the plasma following administration of therapeutic doses.
The metabolic fate of zalcitabine has not been fully evaluated in humans. Dideoxyuridine (ddU) is the principal metabolite that has been identified for zalcitabine. In both urine and feces, ddU accounts for less than 15% of an oral dose of zalcitabine. Zalcitabine is not metabolized substantially in the liver and is relatively resistant to human cytidine deaminase, a catabolic enzyme that degrades many cytidine derivatives. Because zalcitabine is relatively resistant to degradation by cytidine deaminase, the drug is stable in plasma and resistant to first-pass metabolism in the liver.
Hepatic metabolites have not been observed. The antiviral action of zalcitabine, like that of zidovudine and didanosine, is dependent on phosphorylation and incorporation into DNA. The first step is the formation of zalcitabine monophosphate by the enzyme 2'-deoxycytidine kinase, which is followed by formation of the diphosphate and triphosphate metabolites through the action of the cytosine monophosphate kinase and nucleotide diphosphate kinase enzymes, respectively.
Hepatic.
Route of Elimination: Renal excretion of unchanged drug appears to be the primary route of elimination, accounting for approximately 80% of an intravenous dose and 60% of an orally administered dose within 24 hours after dosing (n=19). Renal clearance exceeds glomerular filtration rate suggesting renal tubular secretion contributes to the elimination of zalcitabine by the kidneys.
Half Life: 2 hours
Biological Half-Life
2 hours
Mean elimination half-life was 1.4 hr (range, 1.0-3.5) /in 23 mildly symptomatic human immunodeficiency virus-infected children (mean age, 4.2 years)/.
... The plasma half-time is reported to be 1-2.7 hours.
Toxicity/Toxicokinetics
Toxicity Summary
Zalcitabine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Within cells, zalcitabine is converted to its active metabolite, dideoxycytidine 5'-triphosphate (ddCTP), by the sequential action of cellular enzymes. ddCTP interferes with viral RNA-directed DNA polymerase (reverse transcriptase) by competing for utilization of the natural substrate deoxycytidine 5'-triphosphate (dCTP), as well as incorpating into viral DNA. Due to it's lack of a 3'-OH group, the formation of a 5' to 3' phosphodiester linkage that is necessary for DNA chain elongation is inhibited, thus leading to the termination of viral DNA growth.
Protein Binding
Less than 4%
Toxicity Data
Acute overdose: Inadvertent pediatric overdoses have occurred with doses up to 1.5 mg/kg zalcitabine. Chronic overdose: in an initial dose-finding study in which zalcitabine was administered at doses 25 times (0.25 mg/kg every 8 hours) the currently recommended dose, one patient discontinued zalcitabine after 1.5 weeks of treatment subsequent to the development of a rash and fever.
Interactions
At least one fatality secondary to fulminant pancreatitis possibly related to concomitant use of zalcitabine and IV pentamidine has been reported. If parenteral pentamidine is required to treat Pneumocystis carinii pneumonia in a patient receiving zalcitabine, zalcitabine therapy should be discontinued temporarily. Because parenteral pentamidine has a long elimination half-life, zalcitabine therapy should not be reinitiated until 1-2 weeks after parenteral pentamidine therapy has been completed.
Concurrent use of nitrofurantoin with zalcitabine may increase the risk of pancreatitis and peripheral neuropathy; if concurrent use is necessary, patients should be monitored for signs of toxicity and the dose of zalcitabine may need to be reduced.
Medications associated with the development of pancreatitis /alcohol, asparaginase, azathioprine, estrogens, furosemide, methyldopa, intravenous pentamidine, sulfonamides, sulindac, tetracyclines, thiazide diuretics, valproic acid or other drugs associated with pancreatitis/ should be avoided during zalcitabine therapy or, if concurrent use is necessary, used with caution since zalcitabine may cause pancreatitis, which on rare occasion, has been fatal.
These medications /parenteral aminoglycosides, amphotericin B, foscarnet/ may increase the toxicity of zalcitabine by interfering with its renal clearance.
For more Interactions (Complete) data for ZALCITABINE (9 total), please visit the HSDB record page.
References

[1]. Zalcitabine. An update of its pharmacodynamic and pharmacokinetic properties and clinical efficacy in the management of HIV infection.Drugs. 1997 Jun;53(6):1054-80.

[2]. Interaction of zalcitabine with human organic anion transporter 1. Pharmazie. 2006 May;61(5):491-2.

Additional Infomation
Zalcitabine can cause cancer according to California Labor Code.
2',3'-dideoxycytidine is a white crystalline powder. Odorless. (NTP, 1992)
Zalcitabine is a pyrimidine 2',3'-dideoxyribonucleoside compound having cytosine as the nucleobase. It has a role as an antiviral drug, an antimetabolite and a HIV-1 reverse transcriptase inhibitor.
A dideoxynucleoside compound in which the 3'-hydroxyl group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of 5' to 3' phosphodiester linkages, which are needed for the elongation of DNA chains, thus resulting in the termination of viral DNA growth. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.
Zalcitabine has been reported in Caenorhabditis elegans with data available.
Zalcitabine is a synthetic dideoxynucleoside. After intracellular phosphorylation to its active metabolite, zalcitabine preferentially inhibits the gamma form of DNA polymerase present in tumor cell mitochondria, resulting in the inhibition of tumor cell mitochondrial DNA replication and tumor cell death. (NCI04)
A dideoxynucleoside compound in which the 3'-hydroxyl group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of 5' to 3' phosphodiester linkages, which are needed for the elongation of DNA chains, thus resulting in the termination of viral DNA growth. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.
A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.
Drug Indication
For the treatment of Human immunovirus (HIV) infections in conjunction with other antivirals.
FDA Label
Mechanism of Action
Zalcitabine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Within cells, zalcitabine is converted to its active metabolite, dideoxycytidine 5'-triphosphate (ddCTP), by the sequential action of cellular enzymes. ddCTP interferes with viral RNA-directed DNA polymerase (reverse transcriptase) by competing for utilization of the natural substrate deoxycytidine 5'-triphosphate (dCTP), as well as incorpating into viral DNA. Due to it's lack of a 3'-OH group, the formation of a 5' to 3' phosphodiester linkage that is necessary for DNA chain elongation is inhibited, thus leading to the termination of viral DNA growth.
Zalcitabine enters the cell through carrier-mediated and non-carrier-mediated mechanisms. It is first phosphorylated by deoxycytidine kinase and further by cellular kinases to its active metabolite, dideoxycytidine 5'-triphosphate. Unlike other nucleoside analogs, zalcitabine is most efficiently triphosphorylated in resting peripheral blood mononuclear cells. The triphosphate terminates viral DNA elongation. Zalcitabine decrease the intracellular pool of deoxycytidine triphosphate and binds somewhat to host beta and gamma DNA polymerases.
Therapeutic Uses
Zalcitabine is indicated in combination with zidovudine, for the treatment of HIV infection in patients with limited prior exposure (< 3 months) to zidovudine. Zalcitabine is also indicated, in combination with antiretroviral protease inhibitors, for the treatment of HIV infection. /Included in US product labeling/
Zalcitabine is indicated as a monotherapy for the treatment of advanced HIV infection in patients who are intolerant of, or who have disease progression while receiving, alternative antiretroviral therapy. /Included in US product labeling/
Drug Warnings
Peripheral neuropathy occurring during zalcitabine therapy generally is a sensorimotor neuropathy characterized initially as numbness and burning dysesthesia involving the distal extremities. When manifestations of peripheral neuropathy occur, they often become evident during the first 7-24 weeks of therapy and involve pain and discomfort in the feet, followed several weeks later by a burning dysesthesia in the same area. Clinically, patients may have diminished light touch, pin prick, temperature, and vibration sensations in the area of the feet and up to the midcalf; ankle deep-tendon reflexes may be decreased or absent. If the drug is not discontinued when these initial manifestations appear, sharp shooting pains or severe continuous burning pain may occur and can progress to severe pain requiring opiate analgesics and is potentially irreversible. Discomfort may be severe enough to cause gait disturbances. In some patients, manifestations of peripheral neuropathy progress to include the hands and are sometimes described as occurring in a stocking-and-glove pattern. Nerve biopsy and electrophysical studies indicate that axonal degeneration may occur.
Lactic acidosis and severe hepatomegaly with steatosis (sometimes fatal) have been reported rarely in patients receiving zalcitabine and also have been reported in patients receiving other nucleoside reverse transcriptase agents. Most reported cases have involved women; obesity and long-term therapy with a nucleoside antiretroviral also may be risk factors.
Moderate to severe peripheral neuropathy has been reported in 3-35% of patients receiving oral zalcitabine at usual dosage (0.75 mg every 8 hours) either alone or in conjunction with zidovudine. Peripheral neuropathy occurs more frequently in patients with advanced HIV infection than in those with less advanced disease.
The duration of clinical benefit from antiretroviral therapy may be limited. Alterations in antiretroviral therapy should be considered if disease progression occurs during treatment with zalcitabine.
For more Drug Warnings (Complete) data for ZALCITABINE (33 total), please visit the HSDB record page.
Pharmacodynamics
Zalcitabine is an analog of 2'-deoxycytidine that is pharmacologically related to but structurally different from other nucleotide reverse transcriptase inhibitors (NRTIs). Zalcitabine inhibits the activity of HIV-1 reverse transcriptase (RT) both by competing with the natural substrate dGTP and by its incorporation into viral DNA.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C9H13N3O3
Molecular Weight
211.22
Exact Mass
211.095
Elemental Analysis
C, 51.18; H, 6.20; N, 19.89; O, 22.72
CAS #
7481-89-2
Related CAS #
7481-89-2
PubChem CID
24066
Appearance
Crystals from ethanol and benzene
White to off-white powder
Density
1.6±0.1 g/cm3
Boiling Point
415.0±55.0 °C at 760 mmHg
Melting Point
217-218 °C(lit.)
Flash Point
204.8±31.5 °C
Vapour Pressure
0.0±2.2 mmHg at 25°C
Index of Refraction
1.686
LogP
-1.3
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
3
Rotatable Bond Count
2
Heavy Atom Count
15
Complexity
327
Defined Atom Stereocenter Count
2
SMILES
O1[C@]([H])(C([H])([H])O[H])C([H])([H])C([H])([H])[C@]1([H])N1C(N=C(C([H])=C1[H])N([H])[H])=O
InChi Key
WREGKURFCTUGRC-POYBYMJQSA-N
InChi Code
InChI=1S/C9H13N3O3/c10-7-3-4-12(9(14)11-7)8-2-1-6(5-13)15-8/h3-4,6,8,13H,1-2,5H2,(H2,10,11,14)/t6-,8+/m0/s1
Chemical Name
4-amino-1-((2R,5S)-5-(hydroxymethyl)tetrahydrofuran-2-yl)pyrimidin-2(1H)-one
Synonyms
ddC; Dideoxycytidine; 2'',3''-Dideoxycytidine; Ro 24-2027/000; Ro-24-2027/000; Ro 24-2027 000; NSC606170; NSC 606170; NSC-606170; Zalcitabine; ddC; zalcitabine; Dideoxycytidine; 7481-89-2; 2',3'-DIDEOXYCYTIDINE; ddCyd; HIVID; Cytidine, 2',3'-dideoxy-; ddC; dideoxycytidine, Hivid.
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO:42 mg/mL (198.8 mM)
Water:42 mg/mL (198.8 mM)
Ethanol:<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.08 mg/mL (9.85 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.08 mg/mL (9.85 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (9.85 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 4.7344 mL 23.6720 mL 47.3440 mL
5 mM 0.9469 mL 4.7344 mL 9.4688 mL
10 mM 0.4734 mL 2.3672 mL 4.7344 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT00002118 COMPLETED Drug:Zalcitabine HIV Infections Hoffmann-La Roche Not Applicable
NCT00000997 COMPLETED Drug:Zalcitabine HIV Infections National Institute of Allergy
and Infectious Diseases(NIAID)
1988-12 Not Applicable
NCT00002256 COMPLETED Drug:Zalcitabine HIV Infections Hoffmann-La Roche Not Applicable
NCT00000653 COMPLETED Drug:Zalcitabine HIV Infections National Institute of Allergy
and Infectious Diseases(NIAID)
1995-06 Phase 2
NCT00002117 COMPLETED Drug:Zidovudine
Drug:Zalcitabine
HIV Infections Hoffmann-La Roche Phase 3
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