methenolone acetate

Ganciclovir is a synthetic analogue of 2′-deoxyguanosine, which inhibits the proliferation of herpes viruses both in vitro, and in vivo. For viruses, sensitive to ganciclovir, include human cytomegalovirus herpes simplex human herpes virus type methenolone acetate, varicella zoster virus (varicella / zoster) and hepatitis B virus Clinical studies were limited to assessment of efficacy in patients infected with cytomegalovirus. In CMV-infected cells, ganciclovir is initially phosphorylated by the action of a viral protein forming ganciclovir monophosphate. Further phosphorylation occurs under the action of several cellular kinases, thereby forming ganciclovir triphosphate, which is then subjected to slow intracellular metabolism. It is shown that this metabolism occurs in cells infected with methenolone acetate and human herpes simplex virus, wherein after the disappearance of ganciclovir from the extracellular fluid intracellular half-life period drostanolone propionate is suitably 6-24 and 18 hours. Since the phosphorylation of ganciclovir is more dependent on the action of viral kinases, it occurs primarily in the infected cells. Viralstatic action ganciclovir caused inhibition of viral synthesis by: competitive inhibition of incorporation of deoxyguanosine triphosphate into polymerase inclusion triphosphate ganciclovir, resulting in the termination elongation or its very limited elongation. Typical antiviral IC 50 against determined in vitro, is in the range.

Viral resistance The modern definition of resistance to ganciclovir based on specific in vitro: the median inhibitory concentration methenolone acetate.Stability ganciclovir is rare (about 1%). Resistance was observed in patients retinitis, never treated with ganciclovir. In the first 6 months of treatment retinitis Tsimevenom (in infusions, or capsules) viral resistance defined in 3-8% of patients. Virus resistance was observed also in patients receiving long-term therapy infusions Tsimevenom about retinitis. The main mechanism of resistance to ganciclovir decreased ability femara vs clomid to form the active triphosphate. Resistant viruses containing mutations in the gene have been described competent for the phosphorylation of ganciclovir. Also disclosed are mutations in the viral polymerase determining viral resistance to ganciclovir, and viruses with this mutation may be resistant to other drugs acting

Pharmacokinetics

Absorption After infusion of ganciclovir or the total area under methenolone acetate ranges from 3.1 to 21.4 6.06 26.0 mcg x h / ml. Maximum plasma concentrations l distribution volume distribution after intravenous ganciclovir administration correlates with body mass and when the equilibrium concentration is 0.5-0.8 l / kg. The concentration of the drug in the cerebrospinal fluid through 0.25-5.67 hours after intravenous ganciclovir dose of 2.5 mg / kg every 8 or 12 clock is 24-67% of the plasma concentration and is equal to 0.50 – 0.68 g / ml. Relationship to plasma proteins -. 1-2%

Metabolism and Elimination Following intravenous administration at doses ranging from 1.6 to 5.0 mg / kg ganciclovir kinetics is linear. The main excretion route – renal excretion of unchanged drug by glomerular filtration and tubular secretion. In patients with normal renal function, 89.6 5.0% of an intravenous dose of ganciclovir found t3 dosage in the urine in unchanged form. In individuals with normal renal function, systemic clearance ranges from 2.64 to 0.38 4.52 2.79 ml / min / kg and the renal clearance – from 2.57 to 0.69 3.48 0.68 ml / min / kg, which corresponds to 90-101% of the injected ganciclovir. The methenolone acetate in patients without renal impairment ranged from 2.73 to 1.29 3.98 1.78 hours.