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cobicistat + darunavir (G006 / Rezolsta / Prezcobix)

✓ Approved

Johnson & Johnson Services, Inc. · CYP3A4 · Small Molecule

What is cobicistat + darunavir?

cobicistat + darunavir is a small molecule developed by Johnson & Johnson Services, Inc.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesG006, Rezolsta, Prezcobix
CompanyJohnson & Johnson Services, Inc.
Drug ClassSmall Molecule
Molecular TargetCYP3A4,
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Johnson & Johnson Services, Inc.

Mechanism of Action

Molecular Targets

cobicistat + darunavir 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 + darunavir is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsAcquired immunodeficiency syndrome✓ Approved

Related Research Articles

PubMedMicroorganisms2026-08-27

Longitudinal Clinical and Molecular Characterization of a Single Pediatric Case of Vertically Acquired HIV-1 Subtype C with Baseline Resistance to Protease Inhibitors.

Zaher Kawther A KA, El-Daly Mai M MM, Zaki Eitezaz A EA, Alhazmi Mohammad M MM et al.

Transmitted HIV drug resistance can compromise treatment outcomes in children with vertically acquired infection, particularly when baseline resistance testing is unavailable. This case report describes the longitudinal clinical, virological, immunological, and molecular course of a male child diagnosed with vertically acquired HIV-1 subtype C infection, most consistent with mother-to-child transmission. Clinical history, viral load, CD4/CD8 profiles, HIV-1 pol sequencing, phylogenetic analysis, and interpretation were performed using the Stanford HIV Drug Resistance Database (HIVdb). The baseline viral load was 240,993 copies/mL, with a CD4:CD8 ratio of 0.40. Genotypic analysis identified major protease inhibitor resistance mutations V82A and I84I/V, together with M184V. Stanford HIVdb predicted high-level resistance to lopinavir/ritonavir, atazanavir/ritonavir, lamivudine, and emtricitabine; low-level resistance to darunavir/ritonavir and abacavir; and preserved susceptibility to tenofovir, zidovudine, and the evaluated NNRTIs. Initial lopinavir/ritonavir-based regimens failed to achieve sustained virological suppression. Following treatment optimization with an integrase inhibitor-based regimen and subsequent transition to bictegravir/emtricitabine/tenofovir alafenamide (BIC/FTC/TAF), HIV-1 RNA became Target Not Detected (TND) from November 2024 onward. At the latest follow-up, the CD4 count was 877 cells/µL, the CD8 count was 722 cells/µL, and the CD4:CD8 ratio had improved to 1.21, indicating substantial immune recovery. This single-patient case highlights the clinical value of baseline genotypic resistance testing and individualized, genotype-guided antiretroviral therapy in achieving durable virological suppression in pediatric HIV.

PMID 42654980
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PubMedJournal of xenobiotics2026-08-26

Activated Sludge in the Bioremediation of Water Containing SARS-CoV-2 Antivirals.

Lastovčić Dora D, Zirn Ivona I, Jezerčić Tijana T, Bule Možar Kristina K et al.

The increasing presence of SARS-CoV-2 antivirals (SASs) in wastewater threatens aquatic ecosystems, making it necessary to better understand their removal efficiency during biological treatment. This study evaluates the removal percentages, kinetic mechanisms, and toxicity profiles of six SASs, daclatasvir (DCV), darunavir (DRV), favipiravir (FAV), lopinavir (LOP), remdesivir (REM), and ritonavir (RIT), using activated sludge. A full factorial design combined with response surface methodology (RSM) was used to assess the impact of pH, temperature (T), and mixed liquor suspended solids (MLSS) on SAS removal and microbial stability. The results distinguished two dominant removal pathways. DCV and LOP were primarily removed by adsorption, whereas DRV, FAV, REM and RIT were predominantly removed through biodegradation involving enzymatic transformation and bacterial co-metabolism. RSM achieved a desirability score of 0.772 and identified the optimal operating conditions (pH = 6.08, MLSS = 4.41 g/L, and T = 44.99 °C), resulting in removal efficiencies above 93% for all compounds except DRV, which remained the limiting compound with a maximum removal efficiency of 66%. Perturbation analysis showed that all tested factors have a distinct influence on process performance. These established kinetic trends should support further investigations into advanced biological wastewater treatment methods and precise ecotoxicity profiling of emerging biotransformation products.

PMID 42646048
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PubMedReports (MDPI)2026-08-26

Never Too Late: A Case Report of Severe Fanconi Syndrome Developing After More than a Decade of Silent Tenofovir Disoproxil Fumarate Exposure.

Petrakis Vasileios V, Themelidis Dimitrios D, Panopoulou Maria M, Kriki Pelagia P et al.

Background and Clinical Significance: Tenofovir disoproxil fumarate (TDF) is a widely prescribed nucleotide reverse transcriptase inhibitor (NtRTI) for HIV-1 infection. Though generally well-tolerated, proximal renal tubulopathy resulting in full-blown Fanconi syndrome remains a rare but severe complication (<0.1%). Case Presentation: We present the case of a 52-year-old female living with HIV-1 (diagnosed in 1999, CDC stage A3) who had been treated with a TDF-based antiretroviral regimen for 12 years. Upon admission, she complained of progressive bone pain and polyuria over the preceding six months. Laboratory investigations revealed profound hypokalemia, severe hypophosphatemia, hypouricemia, elevated alkaline phosphatase (ALP) and a decline in renal function (creatinine 1.3 mg/dL from a baseline of 0.7 mg/dL). Arterial blood gas (ABG) analysis showed a normal anion gap hyperchloremic metabolic acidosis alongside respiratory acidosis. Urinalysis demonstrated profound glycosuria in the setting of normal blood glucose levels, coupled with increased 24 h urinary excretion of potassium and phosphorus. A bone scintigraphy demonstrated a "super scan" pattern of metabolic etiology, establishing secondary osteomalacia driven by renal phosphate wasting. Secondary hyperparathyroidism and severe vitamin D3 deficiency were also recorded. The diagnosis of TDF-induced Fanconi syndrome was established. TDF was discontinued, and her antiretroviral regimen was modified to tenofovir alafenamide fumarate (TAF), emtricitabine (FTC), darunavir, and ritonavir, combined with vitamin D supplementation. Over a 6-month follow-up period, renal function normalized, electrolyte wasting resolved, and metabolic acidosis completely reversed. Conclusions: This case highlights that TDF-induced proximal tubulopathy can manifest even after a decade of uneventful therapy, particularly when co-administered with a boosted protease inhibitor.

PMID 42647288
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PubMedCureus2026-08-23

Delayed Multisystem Deterioration Following Large-Volume Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Alafenamide Overdose.

Javed Hamzah M HM, Cuello Sebastion S, Omer Muhammad M, Buryk Yaroslav Y

Genvoya is a fixed-dose antiretroviral medication commonly used in the treatment of human immunodeficiency virus (HIV) infection and is generally well tolerated. Severe toxicity following Genvoya overdose has not been well described, and currently available reports generally describe mild clinical courses managed with supportive care alone. We present the case of a 35-year-old male with HIV, hypertension, and amphetamine use who presented after intentional ingestion of approximately 90 tablets of Genvoya in a suicide attempt. He was initially awake, alert, and hemodynamically stable. Over the next 24 hours, however, he developed distributive shock requiring vasopressor support, acute hypoxic respiratory failure requiring high-flow nasal cannula oxygen therapy, metabolic acidosis, QTc prolongation, mild acute kidney injury, and newly reduced systolic cardiac function with an estimated ejection fraction of 25-35%. Chest imaging demonstrated pulmonary edema and volume overload. Infectious workup remained negative throughout admission. The patient was managed with supportive care in the medical intensive care unit and gradually improved over the following days. This case adds to the limited literature describing severe multisystem complications following large-volume Genvoya overdose.

PMID 42633490
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PubMedJournal of acquired immune deficiency syndromes (1999)2026-08-21

Pharmacokinetic modeling to support WHO-weight band dosing of a new pediatric darunavir/ritonavir (120/20 mg) fixed-dose combination tablet for children at least 3 years old and weighing 10 to less than 35 kg.

Abdalla Seef S, Lallemant Marc M, Compagnucci Alexandra A, Nardone Alessandra A et al.

Darunavir boosted with ritonavir (DRV/r) is the preferred HIV protease inhibitor for children, but no child-friendly fixed-dose combination (FDC) exists. A generic DRV/r 120/20 mg FDC tablet (6:1 ratio) is under development; however, dosing guidance across WHO weight bands is lacking. We performed a pharmacokinetic (PK) modeling/simulation study to inform dosing of the DRV/r FDC tablet in children. Darunavir/ritonavir plasma concentration data from three pediatric HIV trials (DELPHI, ARIEL and CHAPAS-4), administered as separate formulations, were pooled to update a pediatirc population PK model. Simulations were performed for children ≥3 years old weighing 10-<35 kg, evaluating doses of the 120/20 mg DRV/r tablets once- and twice daily per WHO-weight bands. The PK target was a geometric mean DRV exposure (AUC0-tau) within 80%-130% of adult values. Data from 162 children 3-16 years old were included. Darunavir PK was described using a 2-compartment model, with differing absorption lag-time between formulations. Clearance and volume of distribution were allometrically scaled according to weight. Alpha-1-acid glycoprotein concentrations inversely influenced DRV clearance. Simulations predicted the following DRV/r doses achieved target exposures: DRV/r once daily: 480/80 mg (4 tablets) from 10 to <14 kg and 600/100 mg (5 tablets) from 14 to <35 kg. DRV/r twice daily: 240/40 mg (2 tablets) from 10 kg to <14 kg; 360/60 mg (3 tablets) from 14 kg to <25 kg; and 480/80 mg (4 tablets) from 25kg to <35 kg. Model-based dosing supports once- and twice-daily of the pediatric DRV/r 120mg/20mg FDC tablet across WHO-weight bands.

PMID 42628112
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PubMedFrontiers in oncology2026-08-19

Targeting MEST using cobicistat as a therapeutic strategy for gastric cancer through suppressing NF-κB signaling.

Cao Hongtai H, Ye Huili H, Zhang Wentao W, Cai Weiwen W et al.

Gastric cancer (GC) constitutes a substantial global public health challenge, and the lack of tractable molecular targets limits therapeutic progress. Mesoderm-Specific Transcript (MEST) has been implicated in tumor-related signaling, yet its functional role and druggability in GC remain undefined. The analyses of GC tissue microarrays and cohorts were performed to evaluate MEST expression and its clinical significance. CRISPR/Cas9-mediated MEST knockout was used to characterize its oncogenic functions in GC cells and xenograft models. Integrated RNA sequencing and pathway analysis was utilized to elucidate signaling pathways under the regulation of MEST. A structure-guided virtual screen combined with SPR binding and phenotypic assays were employed to discover small molecules targeting MEST. The therapeutic effects and mechanism of the lead compound were evaluated using GC cell lines, patient-derived organoids, cell-derived xenograft (CDX), and patient-derived xenograft (PDX) models. MEST expression in GC tissues was elevated and linked to poor prognosis. Functionally, genetic ablation of MEST impaired GC cell proliferation, invasion, migration, and suppressed tumor growth in CDX models. Screening of approved-compound libraries identified cobicistat as a previously unrecognized high-affinity candidate MEST-inhibitory compound. Cobicistat suppressed tumor growth across a panel of preclinical GC models, including cell lines, organoids, CDX and PDX. Mechanistically, MEST may drive GC progression by activating the NF-κB pathway, whereas cobicistat may antagonize MEST binding and blocked NF-κB pathway. MEST functions as a key oncoprotein driving GC progression via NF-κB activation. Cobicistat, a candidate MEST-inhibitory compound, exhibits favorable preclinical efficacy and safety, providing a promising candidate for targeted GC therapy.

PMID 42614207
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