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Vidarabine phosphate Sale

(Synonyms: ara-AMP; ara-A 5'-monophosphate) 目录号 : GC67195

Vidarabine phosphate (Ara-AMP) 是一种抗病毒剂,可抑制慢性乙型肝炎病毒 (HBV) 感染。Vidarabine phosphate 还可以对抗单纯疱疹病毒和水痘带状疱疹病毒。

Vidarabine phosphate Chemical Structure

Cas No.:29984-33-6

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1g
¥404.00
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5g
¥1,307.00
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产品描述

Vidarabine phosphate (Ara-AMP), an antiviral agent, inhibits chronic HBV infection[1][2]. Vidarabine phosphate also against herpes simplex and varicella zoster viruses[3].

[1]. A W Gough, et al. Comparison of the neonatal toxicity of two antiviral agents: vidarabine phosphate and cytarabine. Toxicol Appl Pharmacol. 1982 Oct;66(1):143-52.
[2]. C I Smith, et al. Vidarabine monophosphate and human leukocyte interferon in chronic hepatitis B infection. JAMA. 1982 Apr 23;247(16):2261-5.
[3]. D Kinchington. Recent advances in antiviral therapy. J Clin Pathol. 1999 Feb;52(2):89-94.

Chemical Properties

Cas No. 29984-33-6 SDF Download SDF
别名 ara-AMP; ara-A 5'-monophosphate
分子式 C10H14N5O7P 分子量 347.22
溶解度 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.88 mL 14.4001 mL 28.8002 mL
5 mM 0.576 mL 2.88 mL 5.76 mL
10 mM 0.288 mL 1.44 mL 2.88 mL
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Research Update

Formulation of a stable Vidarabine phosphate injection

Pharm Weekbl Sci 1984 Jun 22;6(3):101-4.PMID:6462876DOI:10.1007/BF01962998.

An injection fluid with Vidarabine phosphate (37.5 mg/ml, pH 7.4) was formulated. After steam sterilization for 20 min at 120 degrees C a 6.1% degradation was observed. No significant (p greater than 0.05) degradation could be observed after heating in steam for 30 min at 100 degrees C and after storage for four months at 4 degrees C. From the results of an investigation of the degradation rate at elevated temperatures a negligible loss of content after a three years' storage period at 4 degrees C could be predicted.

Recent advances in antiviral therapy

Clin Pharm 1986 Dec;5(12):961-76.PMID:3542344doi

Virus replication is described, and the clinical trials and indications for amantadine, rimantadine, vidarabine, Vidarabine phosphate, acyclovir, ribavirin, and other promising antiviral agents are reviewed. Amantadine and rimantadine are useful for the treatment and prophylaxis of viral influenza A infections. Vidarabine is a second-line agent and is effective for the treatment of herpes simplex encephalitis, neonatal herpes simplex types 1 and 2, and varicella-zoster infections. Vidarabine phosphate (also known as vidarabine monophosphate) has a similar spectrum of activity and can be administered in smaller volumes than vidarabine. Acyclovir has demonstrated clinical efficacy for chickenpox, shingles (herpes zoster), genital herpes, and other herpes simplex infections. Acyclovir is also useful for the suppression of herpes infections. Systemically administered ribavirin is indicated for the treatment of Lassa fever. Aerosol ribavirin is effective for the treatment of respiratory syncytial virus pneumonia in children and infants and influenza A infections in adults. Only acyclovir, amantadine, ribavirin, and vidarabine are used in clinical practice. Vidarabine phosphate and investigational agents such as rimantadine, ganciclovir (DHPG, BW B759U), phosphonoformate, and bromovinyl-deoxyuridine (BVDU) need further investigation.

Adenine arabinoside monophosphate (Vidarabine phosphate) in combination with human leukocyte interferon in the treatment of chronic hepatitis B. A randomized, double-blinded, placebo-controlled trial

Ann Intern Med 1987 Sep;107(3):278-85.PMID:2441633DOI:10.7326/0003-4819-107-2-278.

Study objective: To determine the efficacy of adenine arabinoside monophosphate (Ara-AMP Vidarabine phosphate) with or without human leukocyte interferon in chronic hepatitis B. Study design: Randomized, double-blinded, placebo-controlled trial with 6-month treatment and an 18-month follow-up. Setting: Referral-based liver-disease clinics at three university medical centers. Patients: Twenty-five patients with chronic active hepatitis or cirrhosis and 39 with chronic persistent hepatitis. Interventions: Thirteen patients received intramuscular Ara-AMP, 2.5 mg/kg body weight, twice daily, alternated monthly for 6 months with subcutaneous human leukocyte interferon, 5 million units, twice daily. Painful paresthesia of the legs necessitated dosage reduction and early discontinuation of enrollment. Twenty-four patients received intramuscular Ara-AMP, 2.5 mg/kg, twice daily, alternated monthly for 6 months with a matching placebo given subcutaneously twice daily. Twenty-seven patients received placebo by intramuscular and subcutaneous injections twice daily for 6 months. Measurements and main results: Of the 64 patients, 95% had symptomatic and virologic data available and 64% had biopsies at 12 months; at 24 months, 77% had data available and 56% had repeat biopsies. The highest dropout rate was seen in the group receiving Ara-AMP. The group receiving the placebo was less symptomatic (Karnofsky score of 96% compared with 91% in the group receiving Ara-AMP/placebo and 92% in the group receiving Ara-AMP/human leukocyte interferon, p = 0.02) at 12 but not at 24 months. Loss of DNA polymerase, the hepatitis B e antigen, and the serum hepatitis B virus DNA was similar in all three groups. Histologically, erosion of the limiting plate and lobular activity favored Ara-AMP at 12 but not at 24 months and these differences did not result in differences in the histologic diagnosis. Conclusion: These results do not support the use of Ara-AMP and human leukocyte interferon in chronic persistent or chronic active hepatitis B.