Boston, MA -- (SBWIRE) -- 05/30/2013 -- Stribild (HIV) - Forecast and Market Analysis to 2022

Summary

GlobalData has released its new PharmaPoint Drug Evaluation report, "Stribild (HIV) - Forecast and Market Analysis to 2022". Human Immunodeficiency Virus (HIV), the causative agent of AIDS, has claimed millions of lives since its emergence. However, the advent of antiretroviral therapy (ART) has transformed the face of HIV/AIDS from a deadly disease to a manageable chronic condition for most infected individuals. Antiretroviral treatment not only reduces the viral load and reconstitutes immune function, but also decreases infection incidence rates by limiting viral transmission. The treatment algorithm in HIV has characteristically involved multiple drug regimens designed to tackle the virus on different levels. In the recent past, simplified dosing regimens through the emergence of single tablet regimens (STRs) or fixed dose combination (FDC) therapies have become increasingly popular amongst physicians and patients alike by increasing clinical efficacy thresholds and enabling patient compliance.

View Full Report Details and Table of Contents

Gilead's Stribild is a complete, fixed-dose regimen for antiretroviral-treatment-naive adults with HIV. Stribild contains two NRTIs (emtricitabine/FTC and tenofovir disoproxil fumarate/TDF), a novel INI (elvitegravir/ELV) and a novel PK enhancer (cobicistat/COBI). Stribild's mechanism of action includes the following (Stribild prescribing information, 2012).

FTC, a synthetic nucleoside analog of cytidine, inhibits the activity of HIV reverse transcriptase (RT) by competing with a natural substrate deoxycytidine 5'-triphosphate and by being incorporated into nascent viral DNA resulting in the termination of replication.

TDF, an acyclic nucleoside phosphonate diester analog of adenosine monophosphate, is converted into its active form (i.e., tenofovir diphosphate) by normal metabolic processes. Tenofovir diphosphate inhibits the activity of the HIV RT by competing with deoxyadenosine 5'-triphosphate (a natural substrate), and terminating viral replication if the drug is incorporated into the viral DNA.

ELV inhibits the HIV integrase. This blocks HIV from integrating its DNA into host genomic DNA, which prevents HIV from replicating and propagating.

COBI enhances ELV bioavailability by selectively inhibiting cytochrome P450 enzymes of the CYP3A superfamily, which would otherwise decrease the bioavailability and half-life of ELV via metabolism. Cobicistat has no direct anti-HIV activity.

Scope

- Overview of HIV, including epidemiology, etiology, symptoms, diagnosis, pathology and treatment guidelines as well as an overview on the competitive landscape.
- Detailed information on Stribild including product description, safety and efficacy profiles as well as a SWOT analysis.
- Sales forecast for Stribild for the top nine countries from 2012 to 2022.

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