Focus: Gilead Sciences is a $27.1B revenue public biotech leader specializing in HIV/AIDS, hepatitis, oncology, and infectious disease with 18,000 employees. The company maintains market dominance through peak-stage antivirals and is actively expanding into cancer via protein degraders and antibody-drug conjugates.
Gilead offers stability and scale for infectious disease and oncology careers, but revenue concentration and early-stage pipeline require comfort with execution risk and evolving public health scrutiny.
Why Work Here
Dominant market position in HIV ($3.2B BIKTARVY revenue) and hepatitis C with proven drug development track record in infectious disease and oncology
The information on this page is for informational purposes only and should not be used as a substitute for professional medical advice. Drug information is sourced from FDA, DailyMed, and other government databases. Adverse event data from FAERS does not establish causation. Always consult a healthcare professional for medical decisions.
Active M&A strategy ($3.1B Tubulis acquisition in Apr 2026) signals aggressive pipeline expansion and career mobility across modalities
18,000-person scale with 172 active job openings and balanced hiring across Commercial (36), R&D (35), and Medical Affairs (21) suggests broad internal mobility
Watch Out For
46% revenue concentration in BIKTARVY creates organizational dependency on a single franchise with LOE in 2036; pipeline heavy in early-stage programs (mostly Phase 1–2) offers limited near-term catalyst visibility
Recent LA Times coverage criticizing pricing/access for low-income patients signals reputational and regulatory risk that could impact commercial strategy and policy headwinds
Generated by Claude from Gilead Sciences's SEC filings, pipeline programs, hiring velocity, FDA actions, and WARN data. Inference, not editorial — verify before quoting.
Automated analysis based on publicly available data (FDA, SEC, ClinicalTrials.gov). May be incomplete or delayed. This score does not reflect insider knowledge and should not be used as the sole basis for investment or employment decisions.
12.1 Mechanism of Action HEPCLUDEX is an antiviral drug [see ]. 12.2 Pharmacodynamics HEPCLUDEX 8.5 mg once daily was associated with a higher percentage of trial participants with undetectable HDV RNA at Week 144 compared to a lower once daily dose. 12.3 Pharmacokinetics The pharmacokinetic properties of bulevirtide were characterized after intravenous administration in healthy participants, and after subcutaneous administration in healthy participants and participants with chronic HDV infection. The systemic exposure of bulevirtide increased in a more than proportional manner with increasing doses. At steady state, AUC and C max increased by approximately 2-fold compared to the AUC and C max after the first dose. The pharmacokinetic parameters of bulevirtide are provided in . The steady-state PK parameters of bulevirtide (based on population PK analysis of participants with chronic HDV infection) are provided in . Table 2 Pharmacokinetic Parameters of Bulevirtide Absorption % absolute bioavailability 57 T max (h) (range) 3.00 (1.00 - 4.00) Distribution % bound to human plasma proteins > 99 Elimination t 1/2 (h) t 1/2 values refer to mean terminal plasma half-life. (range) 3 (2 - 6) Metabolism Metabolic pathway Bulevirtide, a linear peptide consisting of L-amino acids, is expected to be degraded to smaller peptides and individual amino acids. No active metabolites are expected. Catabolized by peptidases to amino acids Excretion Major route of elimination Excreted as smaller peptides and amino acids Table 3 Steady-State Pharmacokinetic Parameters of Bulevirtide Following Subcutaneous Administration of HEPCLUDEX in Adults with HDV Infection Empirical Bayesian post hoc exposure estimates from Population pharmacokinetic analysis in MYR301 trial, N=100. Parameter Geometric Mean (90% CI) CI=Confidence Interval C max (ng/mL) 184 (160 - 211) AUC 0-24h (ng•h/mL) 1935 (1680 - 2230) Specific Populations Age (18 to 65 years), sex, race (87.5% White, 1.9% Black, 10.3% Asian, 0.2% Other), or body weight (39.7 to 110 kg) did not have a clinically relevant impact on the systemic exposure of bulevirtide. Geriatric Patients The pharmacokinetics of bulevirtide have not been evaluated in elderly participants with HDV infection (65 years of age and older) [see ]. Patients with Renal Impairment In a Phase 1, open-label study in participants without HDV infection, the steady state pharmacokinetics of bulevirtide were similar among participants with normal renal function and participants with severe renal impairment (CrCl 15 to less than 30 mL per minute), and no clinically relevant differences in total bile acid elevations were observed between the two groups. The pharmacokinetics of bulevirtide have not been evaluated in participants with end-stage renal disease (CrCl less than 15 mL per minute), including those on dialysis. As bulevirtide is greater than 99% protein bound, dialysis is not expected to alter exposures of bulevirtide [see ]. Patients with Hepatic Impairment In a Phase 1, open-label study in participants without HDV infection, the steady-state pharmacokinetics of bulevirtide were approximately 27% lower in participants with moderate hepatic impairment (Child-Pugh Class B) than participants with normal hepatic function. The steady state pharmacokinetics of bulevirtide were similar among participants with severe hepatic impairment (Child-Pugh Class C) and participants with normal hepatic function [see ]. Drug Interaction Studies Effect of Bulevirtide on Other Drugs Cytochrome P450 (CYP) Enzymes: In vitro studies have shown, bulevirtide is not an inhibitor of CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, and CYP3A4. Bulevirtide is not an inducer of CYP1A2, CYP2B6, or CYP3A4. Consistent with in vitro results, bulevirtide at steady state did not impact the pharmacokinetics of the CYP3A4 probe substrate midazolam, administered as an oral 30 μg microdose, in clinical drug-interaction studies. Transporter Systems: In vitro studies have shown that no clinically relevant interactions are expected for efflux transporters including MDR1, BCRP, BSEP, MATE1, and MATE2K and uptake transporters including OATP2B1, OAT1, OAT3, OCT1, and OCT2. In vitro studies have shown that bulevirtide inhibits the organic anion transporting polypeptides, OATP1B1 and OATP1B3, with IC 50 values of 0.5 and 8.7 μM, respectively, and taurocholate uptake via NTCP receptors with an IC 50 value of 0.320 μM; however, no clinical drug interaction is expected for OATP1B or NTCP substrates at clinically relevant concentrations of bulevirtide. Steady state exposures of bulevirtide administered once daily did not impact the pharmacokinetics of TDF (at 300 mg) in a dedicated clinical drug-interaction study. Effect of Other Drugs on Bulevirtide Based on the population PK evaluation of drug interactions for bulevirtide, no clinically relevant drug interactions have been observed with PEG-IFNα and TAF or TDF. 12.4 Microbiology Mechanism of Action Bulevirtide is
Source: state DOL filings, aggregated via Big Local News
No active FDA warnings or WARN filings detected; reputational risk from access/pricing criticism (LA Times, Apr 2026) may drive regulatory and political scrutiny but not imminent operational disruption.
Liver international : official journal of the International Association for the Study of the Liver