Adme and pharmacokinetic properties of remdesivir: Its drug interaction potential

On 11 March 2020, the World Health Organization (WHO) classified the Coronavirus Disease 2019 (COVID-19) as a global pandemic, which tested healthcare systems, administrations, and treatment ingenuity across the world. COVID-19 is caused by the novel beta coronavirus Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Since the inception of the pandemic, treatment options have been either limited or ineffective. Remdesivir, a drug originally designed to be used for Ebola virus, has antiviral activity against SARS-CoV-2 and has been included in the COVID-19 treatment regimens. Remdesivir is an adenosine nucleotide analog prodrug that is metabolically activated to a nucleoside triphosphate metabolite (GS-443902). The active nucleoside triphosphate metabolite is incorporated into the SARS-CoV-2 RNA viral chains, preventing its replication. The lack of reported drug development and characterization studies with remdesivir in public domain has created a void where information on the absorption, distribution, metabolism, elimination (ADME) properties, pharmacokinetics (PK), or drug-drug interaction (DDI) is limited. By understanding these properties, clinicians can prevent subtherapeutic and supratherapeutic levels of remdesivir and thus avoid further complications in COVID-19 patients. Remdesivir is metabolized by both cytochrome P450 (CYP) and non-CYP enzymes such as carboxylesterases. In this narrative review, we have evaluated the currently available ADME, PK, and DDI information about remdesivir and have discussed the potential of DDIs between remdesivir and different COVID-19 drug regimens and agents used for comorbidities. Considering the nascent status of remdesivir in the therapeutic domain, extensive future work is needed to formulate safer COVID-19 treatment guidelines involving this medication

Treatment of Disseminated Herpes Zoster Infections

Of all the infectious complications which plague the immunosuppressed patient, viral infections are the least amenable to drug therapy. Disseminated herpes zoster infections are relatively uncommon in immunosuppressed patients, but affect as many as 25 percent of patients with Hodgkin's disease. Herpes zoster infections are caused by the varicella-zoster virus (VZV), a DNA containing virus which is the etiological agent of both chickenpox and shingles. Vidarabine (ara-A) is a synthetic nucleoside which inhibits viral induced DNA-dependent DNA polymerase, and therefore viral replication. While vidarabine is remarkably nontoxic at a daily dose of 10 mg/kg, there is at present little evidence that early therapy of disseminated herpes zoster prevents visceral disease, further dissemination, or affects the incidence of postherpetic neuralgia. Initial studies employing human leukocyte interferon show promise, but large scale trials have been hampered by limited supplies of interferon. </jats:p

Costs of Pharmaceutical Care: Can the Profession do Anything?

OBJECTIVE: To review some of the factors that influence the cost of pharmaceuticals and the delivery of pharmaceutical care as well as some possible measures for decreasing these costs. DATA SYNTHESIS: Clinical studies have been selected to illustrate factors that may add to the overall cost of pharmaceutical care. CONCLUSIONS: Because of the perceived problems resulting from the introduction of new, expensive pharmaceuticals, possible means of controlling the costs of individual products are discussed. In addition, recommendations for achieving cooperation between pharmaceutical manufacturers and pharmacy practitioners in demonstrating the cost-effectiveness of new products are provided. </jats:sec