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Acyclovir

Acyclovir Suppliers list
Company Name: Zhengzhou Yuanli Biological Technology Co., Ltd
Tel: 0086-371-67897895
Email: info@zzyuanli.cn
Products Intro: Product Name:Acyclovir
CAS:59277-89-3
Purity:0.99 Package:As per customer requirements
Company Name: Chemwill Asia Co.,Ltd.
Tel: 86-21-51086038
Email: chemwill_asia@126.com;sales@chemwill.com;chemwill@hotmail.com;chemwill@gmail.com
Products Intro: CAS:59277-89-3
Purity:99% Package:5KG;1KG;25KG
Company Name: Capot Chemical Co.,Ltd.
Tel: +86 (0)571-855 867 18
Email: sales@capotchem.com
Products Intro: Product Name:Acyclovir
CAS:59277-89-3
Purity:98% (Min,HPLC) Package:100g;1kg;5kg,10kg,25kg,50kg
Company Name: Shenzhen Sendi Biotechnology Co.Ltd.
Tel: 0755-23311925 18102838259
Email: Abel@chembj.com
Products Intro: Product Name:Acyclovir
CAS:59277-89-3
Purity:99% Package:264/KG
Company Name: Henan DaKen Chemical CO.,LTD.
Tel: +86-371-55531817
Email: info@dakenchem.com
Products Intro: Product Name:Acyclovir
CAS:59277-89-3
Purity:99% Package:100g,500g,1KG,10KG,100KG

Lastest Price from Acyclovir manufacturers

  • Acyclovir
  • US $1.00 / kg
  • 2019-05-13
  • CAS:59277-89-3
  • Min. Order: 1kg
  • Purity: 99%
  • Supply Ability: Customized
  • Aciclovir
  • US $10.00 / KG
  • 2019-01-15
  • CAS:59277-89-3
  • Min. Order: 10UG
  • Purity: 99%
  • Supply Ability: 10MT
Acyclovir Chemical Properties
Melting point 256-257°C
Boiling point 366.71°C (rough estimate)
density 1.3654 (rough estimate)
refractive index 1.8000 (estimate)
storage temp. −20°C
solubility H2O: 0.7 mg/mL
form powder
pkapKa 2.27 (Uncertain);9.25 (Uncertain)
color white
Water Solubility Soluble in 1M HCl at 50mg/ml. Soluble in water at 0.7mg/ml. Also soluble in DMSO
Merck 14,146
Stability:Stable. Incompatible with strong oxidizing agents.
InChIKeyMKUXAQIIEYXACX-UHFFFAOYSA-N
CAS DataBase Reference59277-89-3(CAS DataBase Reference)
Safety Information
Hazard Codes Xi,Xn
Risk Statements 36/37/38-40-20/21/22
Safety Statements 22-24/25-36-26-23
WGK Germany 2
RTECS UP0791400
HazardClass IRRITANT
HS Code 29335990
Hazardous Substances Data59277-89-3(Hazardous Substances Data)
ToxicityLD50 in mice (mg/kg): >10,000 orally; 1000 i.p. (Schaeffer)
MSDS Information
Acyclovir Usage And Synthesis
Chemical Propertieswhite to light yellow crystal powder
Useshypnotic
UsesOrally active acyclic nucleoside with inhibitory activity towards several herpes viruses. Antiviral
DefinitionChEBI: An oxopurine that is guanine substituted by a (2-hydroxyethoxy)methyl substituent at position 9.
Brand nameZovirax (GlaxoSmithKline).
Antimicrobial activityActivity is restricted to viruses of the herpes group. Herpes simplex virus (HSV) types 1 and 2, simian herpes virus B and varicella zoster viruses (VZV) are susceptible to concentrations readily attainable in human plasma. The 50% inhibitory concentration (ID50) is 0.1 μmol for HSV-1 and HSV-2 and 3 μmol for VZV, concentrations much below those toxic to cells. Valaciclovir is metabolized to aciclovir, and has the same antiviral profile. Thymidine-kinase-negative HSV mutants and cytomegalovirus (CMV) do not code for thymidine kinase and are generally resistant. Although Epstein–Barr virus (EBV) may have reduced thymidine kinase activity, its DNA polymerase is susceptible to aciclovir triphosphate and shows intermediate susceptibility. Human herpes viruses 6 and 7 are less susceptible than EBV.
Acquired resistanceMutations in HSV that involve deficient thymidine kinase or an altered substrate are most common; alterations in the DNA polymerase gene also result in resistance. Resistant mutants may be found in wild virus populations; mutants lacking thymidine kinase activity may be readily induced by passage of HSV in the presence of the drug. Resistant strains have mostly been reported in immunocompromised patients, are generally thymidine-kinase negative, and have decreased virulence. Resistant mutants that retain thymidine kinase activity appear to retain virulence. Emergence of resistant HSV strains is less frequent in immunocompetent patients, occurring in about 2% of those receiving prolonged treatment.
General DescriptionAcyclovir, 9-[2-(hydroxyethoxy)methyl]-9H-guanine (Zovirax),is the most effective of a series of acyclic nucleosidesthat possess antiviral activity. In contrast with true nucleosidesthat have a ribose or a deoxyribose sugar attached to apurine or a pyrimidine base, the group attached to the basein acyclovir is similar to an open chain sugar, albeit lackingin hydroxyl groups. The clinically useful antiviral spectrumof acyclovir is limited to herpesviruses. It is most active (invitro) against HSV type 1, about two times less against HSVtype 2, and 10 times less potent against varicella–zostervirus (VZV).
The ultimate effect of acyclovir is the inhibition of viralDNA synthesis. Transport into the cell and monophosphorylationare accomplished by a thymidine kinase that is encodedby the virus itself.The affinity of acyclovir for the viralthymidine kinase is about 200 times that of the correspondingmammalian enzyme.
use: oral and parenteral. Oral acyclovir is used in the initialtreatment of genital herpes and to control mild recurrentepisodes. It has been approved for short-term treatment ofshingles and chickenpox caused by VZV. Intravenous administrationis indicated for initial and recurrent infectionsin immunocompromised patients and for the prevention andtreatment of severe episodes. The drug is absorbed slowlyand incompletely from the GI tract, and its oral bioavailabilityis only 15% to 30%. Nevertheless, acyclovir is distributedto virtually all body compartments.
Pharmaceutical ApplicationsA synthetic acyclic purine nucleoside analog of the natural nucleoside 2′ deoxyguanosine, formulated for oral and topical use, and as the sodium salt for intravenous infusion. Valaciclovir (the l-valyl ester) is a prodrug formulation supplied as the hydrochloride for oral use.
Biological ActivityAntiviral agent, active against herpes simplex viruses HSV-1 and HSV-2 (EC 50 values are 0.85 and 0.86 μ M respectively). Interferes with viral DNA polymerization through competitive inhibition with guanosine triphosphate. Induces apoptosis in cells transfected with HSV-TK (suicidal gene therapy).
PharmacokineticsOral absorption, aciclovir: c. 20%
valaciclovir: c. 60%
Cmax 200 mg oral 4-hourly:1.4–4 μmol after 1.5–1.75 h
5 mg/kg 8-hourly intravenous infusion: 43.2 μmol steady state
10 mg/kg 8-hourly intravenous infusion: 88.9 μmol steady state
Plasma half-life: 3–3.3 h
Plasma protein binding: 15%
Absorption
Therapeutic drug levels are readily attained after oral or intravenous administration, although concentrations achieved by an oral dose are over 90% lower than those after intravenous therapy. Accumulation of the drug is unlikely in patients without renal dysfunction. Valaciclovir is readily absorbed and is converted rapidly and almost completely to aciclovir; absorption is unaffected by food. Peak plasma concentrations of 22 μmol are found in subjects after an oral dose of 1000 mg every 8 h; systemic exposure is comparable to that of intravenous aciclovir 5 mg/kg every 8 h. The peak plasma concentration and area under the concentration–time curve (AUC) do not increase proportionally with increasing doses, presumably due to reduced absorption. The time to peak aciclovir concentration is also dose dependent, ranging from 0.9 to 1.8 h after single oral doses of 100–1000 mg.
Distribution
Aciclovir is widely distributed in various tissues and body fluids. Delivery of the drug to the basal epidermis after topical administration is about 30–50% of that obtained by oral dosing. Aciclovir ointment penetrates the corneal epithelium. CSF concentrations are about 50% of simultaneous plasma concentrations. Vesicular fluid concentrations approximate those in plasma. The drug is actively secreted into breast milk at a concentration several times that of plasma. Placental cord blood contains levels of 69–99% of maternal plasma and the drug is 3–6 times more concentrated in amniotic fluid.
Metabolism
About 15% of an intravenous dose is metabolized in persons with normal renal function. The only significant urinary metabolite is 9-carboxymethoxymethylguanine, which has no antiviral activity. Less than 0.2% of the dose is recovered as the 8-hydroxylation product.
Excretion
Around 45–79% of a dose is recovered unchanged in urine, the percentage declining with decreasing creatinine clearance. In patients with renal failure, mean peak plasma concentrations nearly doubled and the elimination half-life increased to 19.5 h. Dosage reductions are advised for various stages of renal impairment. During hemodialysis the half-life is 5.7 h and after dialysis the plasma concentration is about 60% less than the predialysis concentration. Half-lives of 12–17 h have been reported for patients undergoing continuous peritoneal dialysis, with only 13% or less of administered drug being recovered in the 24-h dialysate. The half-life in patients undergoing arteriovenous hemofiltration/dialysis is about 20 h. Less than 1% of a dose of valaciclovir is recovered as unchanged drug in the urine. In multidose studies the amount of aciclovir recovered across dose levels ranged from about 40% to 50%. Between 7% and 12% of the dose is found as the 9-carboxymethoxymethylguanine metabolite. Overall, aciclovir accounts for 80–85% of total urinary recovery.
Clinical UseAciclovir
Herpes simplex keratitis
Chickenpox and herpes zoster
Herpes simplex encephalitis and neonatal herpes
Prophylaxis of HSV infections in the severely immunocompromised
Valaciclovir
Herpes zoster and genital HSV infections
Side effectsFew adverse reactions to topical, ocular, oral or intravenous formulations have been reported. Allergic contact dermatitis occasionally occurs with aciclovir cream. Superficial punctate keratopathy occurs in 10% of patients receiving the ophthalmic preparation; stinging or burning on application occurs in 4%. Less common complications include conjunctivitis, blepharitis and pain.
Transient increases in blood urea nitrogen and creatinine occur in 10% of patients given bolus injections. It can be largely avoided by reducing the rate of infusion, adequate hydration and dosage adjustment in renal failure. Nausea, vomiting, diarrhea and abdominal pain occasionally occur, particularly in association with a raised creatinine concentration. Acute reversible renal failure has been reported. Reconstituted aciclovir has a pH of about 11; severe inflammation and ulceration have been reported after extravasation at the infusion site. Encephalopathy, tremors, confusion, hallucinations, convulsions, psychiatric disorders, bone marrow depression and abnormal liver function have occasionally arisen. Skin rashes have been reported in a few patients but resolve on discontinuation of the drug.
Headache and nausea have been reported as side effects of valaciclovir, but occurred with similar frequency in subjects taking placebo.
Results of mutagenicity tests in vitro and in vivo indicate that aciclovir is unlikely to pose a genetic risk to humans, and the drug was not found to be carcinogenic in long-term studies in mice and rats. No detectable drug-related effects have been detected in pregnancy.
Enzyme inhibitorThis guanosine analogue (FW = 225.21 g/mol; CAS 59277-89-3), also known as acycloguanosine and 9- (2 hydroxyethoxymethyl) guanine, is a widely used and highly effective pro-drug for the treatment of herpes infections . Once transported in cells, where it is metabolically phosphorylated by viral thymidine kinases to the monophosphate and then to to the di- and triphosphate by host cell guanylate kinase and nucleoside 5’-diphosphokinase, acyclovir becomes a potent inhibitor of viral DNA polymerases, with minimal host toxicity. The triphosphate halts viral replication via inhibition of viral DNA polymerases, attended by incorporation and termination of growing viral DNA chains. The selectivity of acyclovir action was investigated by Gertrude Elion and coworkers (Elion shared the 1988 Nobel Prize in Physiology or Medicine). Target (s) : viral DNA polymerases, via the 5’-triphosphate (1-4); HSV-1 replication; varicella zoster virus replication; murine cytomegalovirus DNA polymerase; purine-nucleoside phosphorylase ; thymidine kinase; glycine N-methyltransferase, weakly inhibited; tryptophan 2,3-dioxygenase. Key Pharmacokinetic Parameters: After intravenous dosing of patients with normal renal function, 8–14% of the dose is recovered in the urine as the metabolite 9- carboxymethoxymethylguanine. Adequate distribution of acyclovir occurs in the cerebrospinal fluid, vesicular fluid, vaginal secretions and tissues. The low plasma protein binding of acyclovir precludes drug interactions involving binding displacement. When IV doses in the range of 2.5–15 mg/kg are given every 8 h to adult patients, dose-independent kinetics iss observed. Continuous infusions of acyclovir over an equivalent daily dose range have achieved predictable plasma levels. Acyclovir half- life and total body clearance are influenced significantly by renal function, and dosage adjustments should be made for patients with impaired renal function. See also Appendix II in Goodman & Gilman’s THE PHARMACOLOGICAL BASIS OF THERAPEUTICS, 12th Edition (Brunton, Chabner & Knollmann, eds.) McGraw-Hill Medical, New York. For addition information on acyclovir’s PK properties.
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