Other side effects include fever, trouble sleeping, peripheral neuropathy, and retinal detachment.Of note, the FDA issued several black box warnings concerning potential severe toxicities. These include:

Blood toxicities: neutropenia, anemia, thrombocytopenia
Impairment of fertility (based on animal studies only)
Fetal toxicities (based on animal studies only)
Mutagenesis and carcinogenesis (based on animal studies only)

Drug interactions
While not studied in people, it can be assumed that interactions will be similar as those with ganciclovir, since valganciclovir is converted into ganciclovir in the body. Zidovudine may decrease the concentration of ganciclovir, and together the drugs can cause anemia and neutropenia. Probenecid can increase the concentration of ganciclovir, which could increase the chances of ganciclovir toxicity. People with kidney problems could have an increase in both mycophenolate mofetil and ganciclovir concentrations when both drugs are taken together. Ganciclovir can also increase the concentration of didanosine. Mechanism of action
Valganciclovir is a prodrug for ganciclovir, which is a synthetic analog of 2′-deoxy-guanosine. Its structure is the same as ganciclovir, except for the addition of a L-valyl ester at the 5 end of the incomplete deoxyribose ring. The valine increases both the absorption of the drug in the intestines, as well as the bioavailability of the drug once it is absorbed. The L-valyl ester is cleaved by esterases in the intestines and the liver, leaving ganciclovir to be absorbed by the virus-infected cells.Ganciclovir is first phosphorylated to ganciclovir monophosphate by a viral thymidine kinase encoded by the cytomegalovirus (CMV) upon infection. Human cellular kinases further phosphorylate the molecule to create ganciclovir diphosphate, then ganciclovir triphosphate.
These kinases are present in 10-fold greater concentrations in CMV or herpes simplex virus (HSV)-infected cells compared to uninfected human cells, allowing ganciclovir triphosphate to concentrate in infected cells.Ganciclovir triphosphate is a competitive inhibitor of deoxyguanosine triphosphate (dGTP). It is incorporated into viral DNA and preferentially inhibits viral DNA polymerases more than cellular DNA polymerases. Ganciclovir triphosphate serves as a poor substrate for chain elongation. Once incorporated into viral DNA due to its structure similarity to dGTP, chain termination occurs once a single nucleotide is added to the distal hydroxyl group of the incomplete deoxyribose ring of ganciclovir. Pharmacokinetics
Oral bioavailability is approximately 60%. Fatty foods significantly increase the bioavailability and the peak level in the serum. It takes about 2 hours to reach maximum concentrations in the serum. Valganciclovir is eliminated as ganciclovir in the urine, with a half-life of about 4 hours in people with normal kidney function. The mechanism of this drug is activation via a viral protein kinase HCMV UL97 and subsequent phosphorylation by cellular kinases. The phosphotransferase enzyme can likewise activate valganciclovir. Chemistry
The synthesis of valganciclovir has been reviewed. Many routes use ganciclovir as a starting material. Society and culture
Price and patent status
Roches Valcyte is protected by patent. However a generic version manufactured by Japanese-owned Indian company Daiichi-Ranbaxy was found by the District Court of New Jersey, USA not to infringe Roches patent. In November 2014, FDA approved generics by two manufacturers.The price of a four-month course of valganciclovir from Roche is about US$8,500 in high-income countries, $6,000 in India.