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cobicistat + elvitegravir + GS-7340 + emtricitabine (Genvoya)

✓ Approved

Strides Pharma Science Limited · CYP3A4 · Small Molecule

What is cobicistat + elvitegravir + GS-7340 + emtricitabine?

cobicistat + elvitegravir + GS-7340 + emtricitabine is a small molecule developed by Strides Pharma Science Limited. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesGenvoya
CompanyStrides Pharma Science Limited
Drug ClassSmall Molecule
Molecular TargetCYP3A4,
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Strides Pharma Science Limited

Mechanism of Action

Molecular Targets

cobicistat + elvitegravir + GS-7340 + emtricitabine acts on 2 molecular targets:

CYP3A4cytochrome P450 family 3 subfamily A member 4 (CP33, HLP)
gag-pol, HIV-1 (gag-pol)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

cobicistat + elvitegravir + GS-7340 + emtricitabine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsAcquired immunodeficiency syndrome✓ Approved

Related Research Articles

PubMedHealth science reports2026-11-11

Low Level Viremia in Early HIV RNA Kinetics in Naïve People Living With HIV Treated With Bictegravir/Emtricitabine/Tenofovir Alafenamide or Dolutegravir/Abacavir/Lamivudine: An Observational Multicenter Retrospective Study.

Bonadiman Nicola N, Basso Monica M, Rossi Maria Cristina MC, Giobbia Mario M et al.

Integrase inhibitors have a pivotal role in antiviral therapyA quarter of PLWH had LLV after 3 months of treatmentPLWH with LLV had immunological parameters lower than PLWH with virological suppression but comparable to those with partial response.

PMID 43011739
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PubMedThe plant genome2026-11-11

Designed phenotyping for genomic selection.

Yan Weikai W, Bekele Wubishet W, Nilsen Kirby T KT

Genomic selection (GS) is increasingly used in plant breeding to predict genetic merit using genome-wide molecular markers. While advances in high-throughput genotyping and statistical modeling, including machine learning, have made GS operational across many crop species, realized prediction accuracy continues to vary substantially among traits, environments, and breeding programs. Much of the GS literature has focused on markers and models, whereas comparatively less attention has been devoted to the design of the phenotyping systems that generate the information required for model training. In this perspective, we argue that GS is built on an information-generation system in which breeding and phenotyping generate information, whereas genotyping and modeling capture, utilize, and propagate that information. We propose the concept of designed phenotyping, in which genomic prediction accuracy is constrained by two complementary factors: phenotypic information quality and information transferability. Multi-environment trial design primarily determines phenotypic information quality through its effects on entry-mean heritability, whereas training population design influences both information quality and transferability through its effects on genetic variability, connectivity, relatedness, and relevance. Together, these factors define the practical upper limit of genomic prediction accuracy. We further argue that phenotyping for GS should not be viewed as a one-time activity but as a continuous investment in the information-generation system underlying future genetic gain. Consequently, designed phenotyping represents a strategic framework for integrating trial design and training population design to sustain long-term breeding progress.

PMID 43010584
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PubMedMedicine2026-11-11

Syphilitic proctitis with profuse rectal bleeding in an HIV-infected patient with preserved CD4 count (case report).

Mosi Mohamad H MH, Alfarra Hisham H, Davi Chandni C, Saaki Shaila S et al.

Syphilitic proctitis is an uncommon and frequently under-recognized manifestation of Treponema pallidum infection that can closely mimic inflammatory, infectious, or neoplastic rectal disease. We report an unusually severe, hemorrhagic presentation in a patient with human immunodeficiency virus (HIV) and a preserved cluster of differentiation 4 (CD4) count, a setting in which overlapping etiologies often delay the diagnosis. A heterosexual man in his early 50s with untreated HIV infection and chronic hepatitis B-related cirrhosis (Child-Pugh class B) presented with sudden onset of profuse hematochezia, watery diarrhea, abdominal cramping, and fatigue. Computed tomography angiography revealed pronounced rectal wall thickening with deep ulceration. Colonoscopy demonstrated an indurated, ulcerated rectal lesion, and biopsy showed dense lymphoplasmacytic inflammation, with spirochetes confirmed by T pallidum immunohistochemistry. Negative cytomegalovirus (CMV) immunohistochemistry, undetectable CMV DNA in plasma and rectal tissue, and a preserved CD4 count (445 cells/µL) made CMV proctitis unlikely. The overall clinical, endoscopic, and histologic findings supported a diagnosis of syphilitic proctitis. Management included doxycycline 100 mg twice daily for 2 weeks, selected because of the patient's documented penicillin allergy. Antiretroviral therapy with bictegravir/tenofovir alafenamide/emtricitabine was initiated to treat HIV and provide concurrent hepatitis B coverage. Within 2 weeks, the patient experienced complete resolution of hematochezia and diarrhea. At 3-month follow-up, the CD4 count had risen to 570 cells/µL, HIV RNA was undetectable (<20 copies/mL), and the rapid plasma reagin titer had declined from 1:512 to 1:32. This case underscores that syphilitic proctitis may manifest with severe ulcerative disease even in patients with relatively preserved immune function. Clinicians should maintain vigilance for syphilis in individuals with HIV who present with rectal bleeding or proctitis to prevent diagnostic delays and ensure timely therapy.

PMID 43012798
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PubMedCureus2026-11-11

Lenacapavir in the Treatment and Prevention of HIV-1 Infection: A Narrative Review of Clinical Efficacy and Resistance Selection Risk.

Tasbas Umut U

Lenacapavir is a first-in-class HIV-1 capsid inhibitor. By acting on a structural protein rather than a viral enzyme, it inhibits several stages of the replication cycle and shows no cross-resistance with the available drug classes; a half-life of 8-12 weeks after subcutaneous administration allows a six-monthly regimen. A narrative review was conducted, searching PubMed and ClinicalTrials.gov up to July 2026 and drawing on phase 2 and phase 3 trials, structural and modelling studies, and regulatory documents. In virologically suppressed adults undergoing a planned regimen switch, the week-48 treatment differences for bictegravir/lenacapavir (ARTISTRY-1 and ARTISTRY-2) and for weekly oral islatravir/lenacapavir (ISLEND-1 and ISLEND-2) ranged from -1.0 to 0.3 percentage points, with the upper bound of each 95% confidence interval lying below the prespecified non-inferiority margin of 4 percentage points. These are investigational switch regimens: lenacapavir itself is currently approved only for multidrug-resistant HIV-1 infection and for pre-exposure prophylaxis, whereas neither the bictegravir/lenacapavir nor the islatravir/lenacapavir combination has yet been authorised. In multidrug-resistant infection, 85% of participants in CAPELLA had HIV-1 RNA < 50 copies/mL at week 156 when missing data were excluded. In prevention, no infection occurred among the 2,134 participants in the lenacapavir arm of PURPOSE 1 (0.00/100 person-years; incidence rate ratio vs background: 0.00, 95% CI: 0.00-0.04), whereas the incidence in the emtricitabine-tenofovir alafenamide arm did not differ from the background incidence (incidence rate ratio: 0.84, 95% CI: 0.55-1.28). The pharmacokinetic property that gives lenacapavir its strength is argued to be, at the same time, its principal vulnerability. As a pharmacological concern, the subtherapeutic concentration tail can create a state of functional monotherapy in which resistance may be selected when the virus replicates at concentrations that suppress the wild-type but not a resistant variant (the mutant selection window). Modelling predicts de novo resistance 106-235 days after the last injection and, for N74D and the double mutants, a selection window overlapping even the steady-state concentrations of the six-monthly regimen, so that these mutants may be selected not only during the post-discontinuation tail but also while dosing continues as planned. Resistance actually observed in clinical studies has been limited and conditional: N74D arose in the two participants infected in the lenacapavir arm of PURPOSE 2 despite expected drug concentrations, and in CAPELLA every participant who developed resistance had a background regimen that was inactive or inadequately taken, indicating that the vulnerability is manageable. Lenacapavir therefore requires careful patient selection, fully active companion drugs, and a planned discontinuation strategy.

PMID 43011617
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PubMedBMC medical genomics2026-11-10

Real-world comparison of genome- and exome-based diagnostic workflows in a pediatric Albanian rare disease cohort.

Cullufi Paskal P, Tabaku Mirela M, Skrahin Aliaksandr A, Tomori Sonila S et al.

Pediatric rare diseases are clinically and genetically heterogeneous, often resulting in delayed molecular diagnosis. In routine clinical practice, diagnostic outcomes reflect the combined performance of complete workflows that may differ in sample source, sequencing depth, laboratory procedures, bioinformatics, interpretation, and reporting. We compared two independent clinical diagnostic workflows applied in parallel to the same Albanian pediatric cohort. Seventy-two patients with suspected rare genetic disorders underwent genome sequencing (GS) from saliva or buccal swabs at approximately 30 × mean depth and exome sequencing (ES) from dried blood spots, with more than 98% of target bases covered at ≥20×. The ISO-accredited laboratories independently performed sequencing, analysis, interpretation, and reporting. We assessed report-level primary diagnostic yield, paired outcomes, variant classes, discordant findings, and laboratory-reported secondary/additional findings. Variants of uncertain significance (VUS) were excluded from yield. Raw data were not centrally reanalyzed, and sample types were not cross-tested. At least one workflow reported a pathogenic or likely pathogenic finding interpreted as a primary molecular diagnosis in 29/72 patients (40.3%; 95% CI, 28.9-52.5). GS reports contained primary diagnoses for 26/72 patients (36.1%; 95% CI, 25.1-48.3) and ES reports for 16/72 (22.2%; 95% CI, 13.3-33.6). Primary outcomes were concordant in 56 participants (13 positive and 43 negative) and discordant in 16 (13 GS-only and three ES-only). The GS laboratory also reported 13 secondary/additional variant-level rows in 11 patients (12 P/LP rows and one VUS row), including seven patients without a primary diagnosis. The workflows produced overlapping but non-identical clinical reports, and neither workflow was comprehensive. The observed differences cannot be attributed to sequencing technology alone because sample type, depth, laboratory, bioinformatics, prioritization, and reporting scope were not harmonized. Implementation decisions should integrate diagnostic contribution with cost, turnaround time, infrastructure, workforce, governance, and local feasibility.

PMID 43004392
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PubMedInvestigative ophthalmology & visual science2026-11-10

Volumetric Quantification of Retinal Ischemic Perivascular Lesions (RIPLs) in Coronary Artery Disease.

Jeremic Natasa N, Arabi Sina S, Apata Michael M, Kaya Musa B MB et al.

Retinal ischemic perivascular lesions (RIPLs) have been reported as correlates of several systemic conditions. This study aimed to assess the prevalence, number, area, and volume of RIPLs and to evaluate their association with coronary artery disease (CAD) using a contemporary imaged coronary angiography (CA) cohort. CA patients were imaged using an SS-OCTA device during the same visit. Structural volumes comprising 500 B-scans were pixel-wise annotated by three graders. RIPLs were quantified by presence, count, area and volume for the first time. CAD severity was assessed using the Gensini score (GS). Associations between RIPL metrics and CAD were analyzed using generalized estimating equation models. Multivariable and age and sex adjusted models were calculated. Multiple testing corrections were applied to primary analyses. RIPLs were detected in 38.0% of eyes. In models with the Gensini score (GS) as outcome, RIPL metrics showed weak and inconsistent trends and were not statistically significant, especially after adjustment. The GS showed no significant associations with RIPL presence (β = 0.132, P = 0.102), area (β = 0.173, P = 0.093), count (β = 0.023, P = 0.165), or volume (β = 0.240, P = 0.085) either. Cardiovascular risk factors were not independently associated with RIPL metrics. Those negative findings remained consistent in sensitivity analyses using the SYNTAX II and SCORE2. In this contemporary coronary angiography cohort with high-density OCT imaging, RIPL burden was not significantly associated with CAD and no robust or proportional association with CAD severity was found. In this work, no other disease specific associations could be established.

PMID 43006988
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