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Basic information Antiviral drugs Anti-tumor drug Pharmacokinetics Dosing instructions Dosage Side effects Function Category Toxicity grading Acute toxicity Stimulus data Flammability hazard characteristics Storage Characteristics Extinguishing agent Safety Supplier Related

Cytarabine Basic information

Product Name:
  • cytrarabine
  • Cytosine β-D-arabinofuranoside ,98%
  • DEPOCYT (cytarabine)
  • 4-aMino-1-[(2R,3S,4S,5R)-3,4-dihydroxy-5-(hydroxyMethyl)oxolan-2-yl]-1,2-dihydropyriMidin-2-one
  • 4-Amino-1-beta-D-arabinofuranosyl-2(1H)-pyrimidinone Arabinocytidine Cytosine beta-D-Arabinofuranoside Ara-C
  • Cytarabine for Injection
  • 4-AMino-1-((2R,3S,4S,5R)-3,4-dihydroxy-5-(hydroxyMethyl)tetrahydrofuran-2-yl)pyriMidin-2(1H)-one
  • Ara-cell
Product Categories:
  • API intermediates
  • Antivirals for Research and Experimental Use
  • Biochemistry
  • Chemical Reagents for Pharmacology Research
  • Nucleosides and their analogs
  • Nucleosides, Nucleotides & Related Reagents
  • Active Pharmaceutical Ingredients
  • Bases & Related Reagents
  • Carbohydrates & Derivatives
  • Nucleotides
  • Anti-cancer&immunity
  • API
Mol File:

Cytarabine Chemical Properties

Melting point:
214 °C
D24 +153° (c = 0.5 in water)
Boiling point:
386.09°C (rough estimate)
1.3686 (rough estimate)
refractive index 
1.5100 (estimate)
storage temp. 
H2O: 50 mg/mL, clear, colorless
pKa 4.3 (Uncertain)
Prisms from EtOH (aq)
Water Solubility 
almost transparency
Stable for 1 year as supplied from date of purchase. Solutions in DMSO or water may be stored at -20°C for up to 1 month.
CAS DataBase Reference
147-94-4(CAS DataBase Reference)
EPA Substance Registry System
Cytarabine (147-94-4)

Safety Information

Hazard Codes 
Risk Statements 
Safety Statements 
WGK Germany 
HS Code 
Hazardous Substances Data
147-94-4(Hazardous Substances Data)
LD50 oral in rat: > 5gm/kg



Cytarabine Usage And Synthesis

Antiviral drugs

Cytarabine is a kind of purine nucleoside-class antiviral chemical synthesis that initially extracted from the medium of streptomyces, and then produced from chemical synthesis. It is a white crystalline powder and is very slightly soluble in water. Its monophosphate ester is easily soluble in water. It has inhibitory effect on various kinds of DNA virus such as Herpes simplex virus HSV1 and HSV2, hepatitis B virus, varicella-zoster virus and cytomegalovirus however has no effect on the smallpox virus, adenovirus, and other kinds of DNA or RNA viruses, bacteria and fungi. The exact mechanism of the antiviral effect of cytarabine is currently not fully understood. The mechanism is primarily related to inhibition of viral replication. The drugs and their metabolites can inhibit the viral DNA synthesis through inhibiting viral DNA polymerase while only a very small amount of the drug itself is incorporated into the viral DNA molecule. In the human body, the antiviral effect of the drugs only partially depends on the host immune function with drugs having no immunosuppression effect. Upon intravenous administration in vivo, 75% to 87% of the drug quickly deaminized into arabinose hypoxanthine through the action of deadenylated deoxygenase, Arabinose hypoxanthine has a significant lower antiviral activity than the prototype, and is rapidly distributed in some parts of the tissues; administer 10 mg of drugs per kg of body weight; the peak value of the plasma concentration of arabinose hypoxanthine is 3~6μ/ml while the peak value of plasma concentration of vidarabine is 0.2~0.4μg/ml. Arabinose hypoxanthine can penetrate through the blood-brain barrier with the cerebrospinal fluid drug concentrations being approximately 1/3 of plasma drug concentration. 41% to 53% of the daily dosage is excreted through urinary in the form of arabinose hypoxanthine. 1% to 3% is excreted out in the form of prototype. Cytarabine is clinically mainly used for the treatment of herpes simplex virus encephalitis as well as being used for treating the herpes zoster and chicken pox of immunosuppressed patients but is invalid in treating cytomegalovirus. It also has certain pharmacological activity of inhibition of hepatitis B virus replication. Topical medication is applied to the treatment of herpes simplex virus keratitis and occasionally used for treating vaccinia virus keratitis.
The above information is edited by the Chemicalbook of Dai Xiongfeng.

Anti-tumor drug

Cytarabine is currently one of the most effective drugs in clinical treatment of acute non-lymphatic myeloid leukaemia. It was first successfully synthesized in 1959 f, and is also presented in the sponge. In 1961, it was found that it has inhibitor effect on in mice S180 sarcoma and leukemia L1210. Cross resistance phenomenon was not observed in animal experiments for cytarabine being used in combination with conventional antineoplastic agents such as 6-thioguanine, methotrexate, prednisone, vincristine, mechlorethamine, cyclophosphamide, daunorubicin, methyl cellosolve acetate gag, fluorouracil and mercaptopurine. This drug belongs to pyrimidine-type anti-metabolite class of anti-tumor agents and having cell cycle specificity with s-phase cells being most sensitive to it. It interferes with the cell proliferation through inhibiting the intracellular DNA synthesis. After entering into the human body, cytarabine is converted into cytarabine triphosphate and cytarabine diphosphate through the phosphorylation reaction catalyzed by kinase. The former one can strongly inhibits the synthesis of DNA polymerase while the later one is capable of inhibiting the conversion between cytidine diphosphate to deoxycytidine diphosphate and thereby inhibiting the synthesis and polymerization of cellular DNA. However, its Inhibitory effect on RNA and protein synthesis is very slight.
It is clinically mainly applied to the treatment of the induction stage and maintenance and consolidation phase of acute lymphoblastic leukemia and non-lymphocytic leukemia, the acute transformation phase of chronic myeloid leukemia and malignant lymphoma. In ophthalmology, it is for the treatment of viral conjunctivitis and epidemic keratitis. It also has certain efficacy in the treatment of head and neck cancer, gastrointestinal cancer and lung cancer; In addition, the drug also has inhibitory effect on the proliferation of herpes simplex virus, smallpox virus, and vaccinia virus as well as the immune response of the body.


The oral administration of drugs yield a low absorption amount, and is also extremely easy to get deaminated and lose function in the action of the cytosine deaminase in the gastrointestinal tract and liver. Therefore, it is not recommended to subject to oral administration. It can be absorbed through intravenous, subcutaneous, intramuscular or intrathecal injection. After intravenous injection, it can be widely distributed in the body fluids, tissues and cells. After intravenous infusion of the drug, there is a moderate amount of drugs which can penetrate through the blood-brain barrier with the cerebrospinal fluid drug concentration being about 40% of the plasma concentration. The drug is mainly metabolized in tissues such as liver and kidney. It is quickly deaminated by the cytosine deaminase to form the inactive uracil arabinoside. In the cerebrospinal fluid, due to relative low content of the deaminase, the domination reaction is very slow. For intravenous administration, the half-life of α-phase is 10 to 15 minutes, with beta phase being 2 to 2.5 hours; for intrathecal administration, the half-life can be extended to 11 hours. Within 24 hours, among the given drug, about 10% of drug is excreted through the kidney while the rest 90% is excreted in the form of uracil cytarabine.

Dosing instructions

1. Upon administration of cytarabine, we should appropriately increase the fluid intake of the patient, so that the urine can be maintained basic. If necessary, the patient can also administer allopurinol in combination in order to prevent the increase of bleeding uric acid and uric acid nephropathy.
2. Though it can cause severe adverse reactions such as nauseas and vomiting upon rapid intravenous injection, the drug has relative slight effect on bone marrow suppression which can be generally tolerated by the patients.
3. The intravenous infusion solution should be diluted to 0.5mg/ml.
4. The prepared injection solution can be stored on the at 4 ℃ (refrigerator) for about seven days. However, at room temperature, it can only be stored for 24 hours.
5. For intrathecal injection of drug, the diluted solution should be free of preservatives.
6. Upon adopting moderate dose or high-dose cytarabine for therapy, some patients may get severe adverse reaction in gastrointestinal and nervous system such as gastrointestinal ulcers, gastrointestinal cystic gas, necrotizing enterocolitis, peripheral neuropathy, brain or cerebellar dysfunction such as personality changes, hypotonia, epilepsy, lethargy, stupor, disorientation, nystagmus, dysarthria, and ataxia; Moreover, hemorrhagic conjunctivitis, skin rashes, hair loss, peeling, severe myocardial disease can also occur.
7. Upon the emergence of various kinds of serious adverse reactions, the drug administration should be discontinued immediately with taking effective measures immediately for treatment. Some patients can be given adrenocorticotropic hormone which may alleviate the adverse reactions caused by moderate-dose or high-dose cytarabine.


Adult Usage:
1, the induction therapy of acute leukemia: often applied in combination with other chemotherapy drugs, 1~3mg/kg each time, intravenous infusion, q: 12h, continuously administer for 5 to 7 days. Repeat at a interval of 1 to 2 weeks.
2, Moderate, large reduction therapy: this is commonly used in the intensive treatment of refractory or relapsed acute leukemia or acute leukemia after remission. For moderate dose: administer 500~1000mg/m2 per time, intravenous infusion of 1 to 3 hours, q12h, 2~6 day as a course. Large doses means 1000~3000mg /m2 per time with similar usage as for moderate dosage. Owing to that the adverse reaction is enhanced with increased dose cytarabine, large doses mainly in turn negatively affect its efficacy, thereby it is now more in favor of moderate dosage protocol.
3, subcutaneous injection: 10mg/m2 per time, q12h, 14~21 as a course of treatment. If the symptom is not alleviated and the patient's condition allows, the treatment can be repeated for another course after 2 to 3 weeks. This protocol can be used for the treatment of myelodysplastic syndrome with increased amount of original cells, low proliferative leukemia, and acute non-lymphocytic leukemia of elderly patients.
4, intrathecal injection: for treating meningeal leukemia, administer 25~75 mg per time; together with 5 mg of dexamethasone; subject to intrathecal injection after using NS for dissolving; administer 1 or 2 times per week until the cerebrospinal fluid (CSF) examination becomes normal. For preventive medicine purpose, administer 1 time in every 4 to 8 weeks.
For children usage: acute leukemia induction therapy, 100mg/(m2 • d), continuously administer for 5 to 7 days.

Side effects

Digestive System: common adverse reactions include loss of appetite, nausea, vomiting, diarrhea, gastritis, stomatitis and gastrointestinal ulcers. Some patients get abnormal liver function, elevated level of bilirubin and aminotransferase. Large-dose treatment can cause significant liver dysfunction and jaundice; it can cause the occlusion of central vein of liver and vein of liver lobule, resulting in jaundice, hepatomegaly, ascites and hepatic encephalopathy.
Blood system: bone marrow suppression increases with increased dose; exhibit as the decrease of leukopenia and thrombocytopenia.
Local reactions: pain at the infusion site and thrombophlebitis mostly disappear after stopping; there are still occasionally reactions such as itching and rashes; treatment of topical ophthalmic drugs can often cause temporary burning, itching and other mild irritation and can also cause tears, foreign body sensation, conjunctival hyperemia, superficial punctate keratitis, pain, photophobia and other reactions.
Central nervous system: occasional discomfort, fatigue, tremors, dizziness, hallucinations, psychotic symptoms and fuzzy sense. These adverse reactions are dose-related and usually disappear after stopping drug. Cases of headache and encephalopathy have also been reported with the later often being difficult for distinguish from protopathy disease can often occurs in the patients with liver and kidney dysfunction.
Overdose performance: when the daily administered cytarabine dose is higher than 20mg/kg, bone marrow suppression can occur; once overdose occur, the patients need to subject to close monitor of the blood system and changes in liver and kidney function .
Other adverse reactions: transient increase in alanine aminotransferase is often observed. Increase of serum total bilirubin also occurs occasionally. Dizziness, fever, hair loss, rash, etc., can also occur. Moreover, it can result in male reproductive dysfunction. Patients of allergy, pregnant women and lactating women should be disabled. Patients with decreased white blood cell count and decreased platelet counts decreased significantly, biliary tract disease, history of gout or urate kidney stones, and who have recently received cytotoxic drugs or radiation therapy, as well as with liver and kidney dysfunction should take with caution.


Ara-C inserts into DNA, and forms complex with topoisomerase I (topoisomerase I) to inhibit DNA replication, causing DNA cleavage. It can’t inhibit RNA synthesis. It can be used as anti-leukemia substance for being used in various types of acute leukemia.


Toxic Substances

Toxicity grading


Acute toxicity

Oral-rat: LD50> 5000 mg/kg; Oral-Mouse LD50: 3150 mg/kg

Stimulus data

Skin-people 45 mg/3 weeks, moderate, three weeks; eyes-people 105 mg/7 days Skin allergy agent

Flammability hazard characteristics

Combustible; combustion produces toxic fumes of nitrogen oxides

Storage Characteristics

Treasury: ventilation, low-temperature and drying; store it separately from food raw materials

Extinguishing agent

Dry powder, foam, sand, carbon dioxide, water spray


Cytarabine (147-94-4) is a nucleoside analog that interferes with DNA synthesis and transcription, particularly in tumor cells.1,2 Cellular enzymes convert it to its nucleotide form, Ara-CTP, which disrupts DNA and RNA synthesis when polymerases attempt to incorporate it.3,4 For the same reasons, it is also employed as an antiviral.5 It inhibits proliferation of a variety of leukemic cell lines (IC50s 16-72 nM), but is used primarily against acute myeloid leukemia (AML).6

Chemical Properties

A white or almost white, crystalline powder, freely soluble in water, very slightly soluble in alcohol and in methylene chloride.




Used as an antineoplastic and antiviral. A selective inhibitro of DNA synthesis. Does not inhibit RNA synthesis


antineoplastic, antiviral, antimetabolite


Cytarabine USP (Cytosar)is used to treat Acute granulocytic leukemia (adults); acute lymphocytic leukemia (children); Hodgkin’s disease


ChEBI: A pyrimidine nucleoside in which cytosine is attached to D-arabinofuranose via a beta-N1-glycosidic bond.


Cytarabine (cytosine arabinoside, ara-C, Cytosar-U) is an analogue of the pyrimidine nucleosides cytidine and deoxycytidine. It is one of the most active agents available for the treatment of acute myelogenous leukemia. Cytarabine kills cells in the S-phase of the cycle by competitively inhibiting DNA polymerase. The drug must first be activated by pyrimidine nucleoside kinases to the triphosphate nucleotide ara-cytosine triphosphate (ara-CTP). The susceptibility of tumor cells to cytarabine is thought to be a reflection of their ability to activate the drug more rapidly (by kinases) than to inactivate it (by deaminases).

Manufacturing Process

(A) Preparation of 1- (2,3,5-Tri-O-Acetyl-β-D-Arabinofuranosyl)-4-Thiouracil: A mixture of 1.85 g (5.0 mmol) of 1-(2,3,5-tri-O-acetyl-β-arabinofuranosyl) uracil, 1.23 g (5.55 mmol) of phosphorus pentasulfide, and 30 ml of pyridine was heated under gentle reflux for 2.5 hours with exclusion of moisture. The reaction mixture was cooled, and the supernatant solution was transferred by means of a pipette into a mixture of crushed ice and water. The reaction flask was washed twice with pyridine, and these washings were added to the icewater mixture. This mixture was kept at about 25°C until the ice had melted, and was then stored at 0°C for one hour. A pale yellow precipitate that formed was collected on a filter, washed with ice-water, and dried in air.
This material was triturated with chloroform, and the chloroform mixture was filtered. A small amount of undissolved material collected on the filter and it was washed with chloroform. The chloroform solution (filtrate plus washings) was washed three times with ice-water, twice with ice-cold 3 N sulfuric acid, twice with ice-cold saturated aqueous sodium bicarbonate solution, twice with ice-water, and then dried over anhydrous sodium sulfate. The chloroform was removed under reduced pressure at a bath temperature of about 40°C, leaving a yellow, somewhat gummy residue. This yellow residue was dissolved in absolute methanol which was then evaporated at reduced pressure at about 40°C, and the residue was then held for 2 hours at 0.5 to 2.0 mm pressure and a bath temperature of about 50°C. There was thus obtained 1.69 g of 1- (2,3,5-tri-O-acetyl-β-D-arabinofuranosyl)-4-thiouracil.
(B) Preparation of 1-β-D-Arabinofuranosylcytosine: In a glass liner, a mixture of 1.16 g (3.0 mmol) of 1-(2,3,5-tri-O-acetyl-β-D-arabinofuranosyl)-4- thiouracil prepared in (A) and about 60 ml of absolute methanol which had been saturated with anhydrous ammonia at 0°C was heated in a steel bomb at 98° to 105°C for 35 hours. After cooling to about 25°C and venting the bomb, the dark solution was filtered into a round-bottom flask. The methanol and excess ammonia were then removed under reduced pressure at about 25°C. The residual syrup was dissolved in absolute methanol, and the methanol was removed under reduced pressure at a bath temperature of about 40°C. This procedure of dissolving in absolute methanol and removing the solvent was repeated, and the residue was held under reduced pressure at a bath temperature of 45°C for 12 hours.
The resulting semisolid was triturated thoroughly with absolute methanol, and the resulting suspension was chilled at 0°C. A pale tan solid that separated was collected on a filter and washed repeatedly with methanol. After washing with anhydrous ether, there was obtained 430 mg of 1-β-Darabinofuranosylcytosine.
(C) Preparation of 1-β-D-Arabinofuranosylcytosine Hydrochloride: The absolute methanolic filtrate obtained after triturating and filtering the 1-β-Darabinofuranosylcytosine in (B) above was warmed and stirred with decolorizing charcoal. The mixture was filtered through a bed of filter aid, and the filter bed was washed repeatedly with absolute methanol. The combined filtrate and washings were pale yellow. The solution was diluted to faint cloudiness with anhydrous ether, and an excess of anhydrous hydrogen chloride was introduced. Crystallization began at about 25°C and further crystallization was induced by chilling at 0°C for 14 hours. The crystalline product was collected on a filter, washed with anhydrous ether, and dried in air. There was thus obtained 180 mg of pale yellow 1-β-Darabinofuranosylcytosine hydrochloride melting at 186° to 189°C.
The pale yellow product was dissolved in warm, absolute methanol, and the solution after mixing with decolorizing charcoal was filtered through a bed of filter aid. The filter bed was washed with warm absolute methanol, and the combined methanolic filtrate and washings were warmed and diluted with anhydrous ether to incipient crystallization. The methanol-ether mixture was kept at about 25°C for about 1 hour and then chilled, first at 0°C, and then at -20°C. The resulting colorless needles were collected on a filter, washed with anhydrous ether, and dried at 85°C, yielding 100 mg of 1-β-Darabinofuranosylcytosine hydrochloride having a melting point of 186° to 188°C.

brand name

Cytosar-U (Sicor); Depocyt (Skyepharma).

Therapeutic Function

Cancer chemotherapy

General Description

Cytarabine is a pyrimidine nucleoside drug that is related toidoxuridine. This agent is primarily used as an anticanceragent for Burkitt lymphoma and myeloid and lymphaticleukemias. Cytarabine blocks the cellular utilization of deoxycytidine,hence inhibiting the replication of viral DNA.Before it becomes active, the drug is converted to monophosphates,diphosphates, and triphosphates, which block DNApolymerase and the C-2 reductase that converts cytidinediphosphate into the deoxy derivative.
The antiviral use of cytarabine is in the treatment of herpeszoster (shingles), herpetic keratitis, and viral infectionsthat resist idoxuridine. Cytarabine is usually administeredtopically. Toxicity occurs on bone marrow, the gastrointestinal(GI) tract, and the kidneys.

General Description

The drug is available in 100-, 500-, 1,000-, and 2,000-mgmultidose vials for IV use. Cytarabine is used in the treatmentof acute myelogenous leukemia and CML. This drugis a deoxycytidine analog originally isolated from thesponge Cryptothethya crypta. It is active following intracellularactivation to the nucleotide metabolite ara-CTP. Theresulting ara-CTP is incorporated into DNA resulting inchain termination and inhibition of DNA synthesis andfunction. Resistance can occur because of decreased activationor transport and increased catabolic breakdown.Metabolic breakdown within the GI tract leads to poorbioavailability. The drug distributes rapidly into tissues andtotal body water with cerebrospinal fluid (CSF) levelsreaching 20% to 40% of those in plasma. Cytidine deaminaseis the primary catabolic enzyme involved in the inactivationof cytarabine. Drug interactions include antagonismof the effects of gentamicin, decreasing the oral bioavailabilityof digoxin, as well as enhancing the cytotoxicity ofvarious alkylating agents, cisplatin, and ionizing radiation.
Toxicities include myelosuppression, leukopenia andthrombocytopenia, nausea and vomiting anorexia, diarrhea,and mucositis. Neurotoxicity is usually expressed as ataxia,lethargy, and confusion. An allergic reaction often describedin pediatric patients includes fever, myalgia, malaise, bonepain, skin rash, conjunctivitis, and chest pain.Pretreatment with methotrexate enhances the formation ofara-CTP metabolites resulting in enhanced cytotoxicity.

General Description

Colorless crystals. Used as an antiviral agent.

Air & Water Reactions

Water soluble.

Health Hazard

ACUTE/CHRONIC HAZARDS: Very toxic. Hazardous decomposition products. May cause irritation on contact. Teratogen. Mutagen. Central nervous system effects.

Biochem/physiol Actions

Ara-C incorporates into DNA and inhibits DNA replication by forming cleavage complexes with topoisomerase I resulting in DNA fragmentation; does not inhibit RNA synthesis. Anti-leukemia agent.

Mechanism of action

Cytarabine is rapidly metabolized in the liver, kidney, intestinal mucosa, and red blood cells and has a half-life in plasma of only 10 minutes after intravenous bolus injection. The major metabolite, uracil arabinoside (ara-U), can be detected in the blood shortly after cytarabine administration. About 80% of a given dose is excreted in the urine within 24 hours, with less than 10% appearing as cytarabine; the remainder is ara-U.When the drug is given by continuous infusion, cytarabine levels in CSF approach 40% of those in plasma.

Clinical Use

Cytarabine is used in the chemotherapy of acute myelogenous leukemia, usually in combination with an anthracycline agent, thioguanine, or both. It is less useful in acute lymphoblastic leukemia and the lymphomas and has no known activity against other tumors. It has been used intrathecally in the treatment of meningeal leukemias and lymphomas as an alternative to methotrexate.

Safety Profile

Moderate to low toxicity byingestion. Human systemic effects: allergic dermatitis,ataxia, blood changes, central nervous system effectsconjunctive irritation, degenerative brain changes, hearingacuity change, lachrymation, peripheral nervefasciculati

Chemical Synthesis

Cytarabine, 4-amino-1-β-arabinofuranosyl-2(1H)pyrimidone (, is made from 1-β-D-arabinofuranosyluracil by preliminary acylation of the hydroxyl group, forming a triacetyl derivative (, and subsequent replacement of the carbonyl group at position 4 of the pyrimidine ring with a thiocarbonyl group using phosphorous pentachloride, and finally replacing the mercapto group of with an amino group using ammonia and simultaneous hydrolysis of the acetyl-substituted groups, giving cytarabine (

Veterinary Drugs and Treatments

In veterinary medicine, cytarabine is used primarily in small animals as an antineoplastic agent for lymphoreticular neoplasms, myeloproliferative disease (leukemias), and CNS lymphoma. Refer to the Dosages below or the Protocols (in the appendix), for more information.

Drug interactions

Potentially hazardous interactions with other drugs
Antipsychotics: avoid with clozapine, increased risk of agranulocytosis.


Cytarabine is converted by phosphorylation to an active form, which is rapidly deaminated, mainly in the liver and the kidneys, by cytidine deaminase to inactive 1-β-darabinofuranosyluracil (uracil arabinoside, ara-U). Approximately 80% of an intravenous dose is excreted in the urine within 24 hours, mostly as the inactive metabolite with about 10% as unchanged cytarabine. A small amount is excreted in the bile.

Purification Methods

Purify cytarabin by recrystallisation from aqueous EtOH or a large volume of H2O (it solubility at ~20o is 5%). It has max 212 and 279nm at pH 2 and 272nm at pH 12. It is an acute leukaemic agent. [Walwick et al. Proc Chem Soc (London) 84 1959, Beilstein 25 III/IV 3669.]


Derissen and Beijnen (2020), Intracellular Pharmacokinetics of Pyrimidine Analogues used in Oncology and the Correlation with Drug Action; Clin. Pharmacokinet., 59 1521 Z Li et al. (2017), Exploring the Antitumor Mechanism of High-Dose Cytarabine through the Metabolic Perturbations of Ribonucleotide and Deoxyribonucleotide in Human Promyelocytic Leukemia HL-60 Cells; Molecules, 22 E499 Zhang & Kiechle (2004), Cytosine Arabinoside Substitution Decreases Transcription Factor-DNA Binding Element Complex Formation; Arch. Pathol. Lab. Med., 128 1364 Renis (1973), Antiviral Activity of Cytarabine in Herpesvirus–Infected Rats; Antimicrob. Agents Chemother., 4 439 Qin et al. (2007), Effect of Cytarabine and Decitabine in Combination in Human Leukemic Cell Lines; Clin. Cancer Res., 13 4225 Walter et al. (2020), Optimal Dosing of Cytarabine in Induction and Post-Remission Therapy of Acute Myeloid Leukemia; Leukemia, 35 295

Cytarabine Preparation Products And Raw materials

Preparation Products


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