Vericiguat 10mg tablets
Requires a prescription from a doctor or prescriber
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Suspected adverse reactions reported for Vericiguat
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Verquvo 10mg tablets
WHO defined daily dose (DDD)
10 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 28 · Randomised trials: 7 · 2020–2026
Showing the 50 most relevant studies, sorted by most relevant.
Urjosee Sahana, Markus Wehland, Ulf Simonsen, et al.
International Journal of Molecular Sciences, 2023
Despite recent advances in heart failure (HF) therapy, the risk of cardiovascular (CV) mortality, morbidity, and HF hospitalization (HFH) are major challenges in HF treatment. We aimed to review the potential of vericiguat as a treatment option for HF. A systematic literature review was performed using the PubMed database and ClinicalTrials.gov. Four randomized controlled trials were identified, which study the safety and efficacy of vericiguat in HF patients. Vericiguat activates soluble guanylate cyclase (sGC) by binding to the beta-subunit, bypassing the requirement for NO-induced activation. The nitric oxide (NO)–sGC–cyclic guanosine monophosphate (cGMP) pathway plays an essential role in cardiovascular (CV) regulation and the protection of healthy cardiac function but is impaired in HF. Vericiguat reduced the risk of CV death and HFH in HF patients with reduced ejection fraction (HFrEF) but showed no therapeutic effect on HF with preserved ejection fraction (HFpEF). The trials demonstrated a favorable safety profile with most common adverse events such as hypotension, syncope, and anemia. Therefore, vericiguat is recommended for patients with HFrEF and a minimum systolic blood pressure of 100 mmHg. Treatment with vericiguat is considered when the individual patient experiences decompensation despite being on guideline-recommended medication, e.g., angiotensin-converting inhibitor/AT1 receptor antagonist, beta-adrenoceptor antagonist, spironolactone, and sodium-glucose transporter 2 inhibitors. Furthermore, larger studies are required to investigate any potential effect of vericiguat in HFpEF patients. Despite the limitations, vericiguat can be recommended for patients with HFrEF, where standard-of-care is insufficient, and the disease worsens.
Abstract licence: CC BY 4.0
van Essen BJ, Ceelen DCH, Ouwerkerk W, et al.
2025
- Stroke Volume
- Heart Failure
- Adrenergic beta-Antagonists
BackgroundIn 2022, a network meta-analysis showed that a combination of β-blockers, angiotensin receptor-neprilysin inhibitors (ARNi), mineralocorticoid receptor antagonists (MRAs), and sodium-glucose cotransporter 2 inhibitors (SGLT2i) was most effective in reducing all-cause mortality in heart failure with reduced ejection fraction (HFrEF). This study updates the treatment benefit by including additional large randomized controlled trials (RCTs) since 2022, including the VICTOR (Vericiguat Global Study in Participants with Chronic Heart Failure) trial.ObjectivesThe goal of this study was to evaluate and compare regimens of pharmacotherapy in patients with HFrEF.MethodsMEDLINE, Embase, and Cochrane Central Register of Controlled Trials databases were searched for RCTs in patients with HFrEF through April 2025. Using frequentist network meta-analysis, HRs for all-cause mortality (primary outcome), cardiovascular death, and the composite of cardiovascular death or heart failure hospitalization (secondary outcomes) were estimated. Absolute benefits were quantified as life-years gained by using BIOSTAT-CHF (Biology Study to Tailored Treatment in Chronic Heart Failure) and ASIAN-HF (Asian Sudden Cardiac Death in Heart Failure) cohort data.ResultsThe analysis included 103,754 patients across 89 randomized controlled trials. Relative to placebo, quintuple therapy with ARNi, β-blockers, MRAs, SGLT2i, and vericiguat most effectively reduced all-cause mortality (HR: 0.35; 95% CI: 0.27-0.45), followed by quadruple therapy with ARNi, β-blockers, MRAs, and SGLT2i (HR: 0.39; 95% CI: 0.32-0.49). For a representative 70-year-old patient, quadruple therapy (ARNi/β-blockers/MRAs/SGLT2i) provided 5.3 additional life-years (95% CI: 2.8-7.7) vs no treatment, while quintuple therapy (ARNi/β-blockers/MRA/SGLT2i/vericiguat) provided 6.0 additional life-years (95% CI: 3.7-8.4).ConclusionsThis analysis reinforces the substantial mortality and morbidity benefit associated with the currently recommended quadruple therapy regimen (ARNi, β-blockers, MRAs, and SGLT2i) in patients with HFrEF. The addition of vericiguat may provide an incremental survival gain of approximately 0.7 year beyond that achieved with quadruple therapy. However, these results should be regarded as exploratory, as they are derived from a secondary endpoint of a single trial.
Abstract licence: CC BY
Dong-Won Kang, Seung-Ho Kang, Kyungmin Lee, et al.
International journal of cardiology, 2024
Meng Wang, Zhihong Zuo, Ting Wu, et al.
Frontiers in Pharmacology, 2026
Abdullah Kilic, Ayushi Saxena, Bilal Khan, et al.
Cureus, 2026
Darmadi Darmadi, Herwindo Ahmad, Cennikon Pakpahan, et al.
Rawal Medical Journal, 2025
Mohamed Bin Zarti, Amna Tamgheli
American Journal of Cardiovascular Drugs, 2024
Nasir YM, Yasmeen J, Shama N, et al.
2026
BackgroundHeart failure (HF) remains a major global health burden, with mortality continuing to rise despite therapeutic advances. Vericiguat, a soluble guanylate cyclase stimulator, has demonstrated potential benefit in patients with worsening HF with reduced ejection fraction (HFrEF), although results across randomized trials have been inconsistent.MethodsWe conducted a systematic literature search across PubMed, Scopus, and ClinicalTrials.gov for relevant articles from inception through September 30th, 2025. Outcomes were reported as pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs). Statistical significance was defined as a 95% confidence interval not crossing 1.0 with a two-tailed p-value ResultsFive randomized controlled trials (RCTs) with 12,877 patients (6857 in the vericiguat group and 6020 in the placebo group) were included. Vericiguat demonstrated a borderline but non-significant reduction in composite outcome of cardiovascular death (CVD) or hospitalization for HF (OR 0.92, 95% CI 0.85-1.00; p = 0.05), hospitalization for HF (OR 0.93, 95% CI 0.85-1.02; p = 0.14), and all-cause mortality (ACM) (OR 0.91, 95% CI 0.81-1.01; p = 0.07).ConclusionThe findings of this study suggest that Vericiguat, when added to guideline-directed medical therapy in patients with heart failure, was associated with a borderline, non-significant reduction in the risk of the composite outcome of cardiovascular death or heart failure hospitalization, as well as all-cause mortality. Further large-scale randomized trials are warranted to better define its clinical benefit.
Abstract licence: CC BY
Batista PG, Dos Santos Silva RRA, Montenegro MV, et al.
2026
Chao Chen, Jin-Xiong Lv, Changzhao Liu
Frontiers in Endocrinology, 2024
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
13 found
Half-life
30 hours
Mechanism
Heart failure (HF) involves, amongst other morphologic and physiologic changes,…
Food interactions
1 warning
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10mg
Half-life
30 hours
[L31153]
Protein binding
98%
[L31153]
Volume of distribution
[L31153]
Metabolism
5%
[L31153]
Other identified metabolites include a denbenzylated compound[A227458] and an M15 metabolite thought to be the result of oxidative metabolism,[A227478] although these metabolites are poorly characterized.
Elimination
53%
[L31153]…
Clearance
1.6 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Vericiguat was approved by the FDA in January 2021 - developed by Merck under the brand name Verquvo - for use in certain patients with systolic heart failure.[L31178] Although not the first sGC stimulator to be granted FDA approval ([riociguat] was approved in 2013 for use in pulmonary hypertension),[L3955] vericiguat is unique amongst its peers in that modifications to its structure have dramatically decreased its susceptibility to oxidative metabolism,[A227458] resulting in a relatively long half-life and allowing for once-daily dosing.
[L31153]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 320 interactions
Dialysis is unlikely to be of benefit in vericiguat overdose given its high degree of protein binding.
[L31153]
Vericiguat directly stimulates sGC by binding to a target site on its beta-subunit,[A227488] bypassing the need for NO-mediated activation, and in doing so causes an increase in the production of intracellular cGMP that results in vascular smooth muscle relaxation and vasodilation.[L31153]
Animal reproduction studies have demonstrated the potential for embryo-fetal toxicity when vericiguat is administered to pregnant females - defects in major vessel and heart formation, as well as spontaneous abortions/resorptions, were observed when vericiguat was administered to pregnant rabbits during organogenesis.[L31153] The possibility of pregnancy should be excluded prior to beginning therapy with vericiguat, and adequate contraception should be used throughout therapy and for one month following cessation of treatment.[L31153]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L31153]
The absolute bioavailability of orally-administered vericiguat is approximately 93% when taken with food - co-administration with meals has been shown to reduce pharmacokinetic variability, increase Tmax to roughly 4 hours, and increase Cmax and AUC by 41% and 44%, respectively.
[L31153]
[L31153]
[L31153]
[L31153]
[L31153]
Other identified metabolites include a denbenzylated compound[A227458] and an M15 metabolite thought to be the result of oxidative metabolism,[A227478] although these metabolites are poorly characterized.
[L31153]
A human mass balance study found that the portion recovered in the urine comprised approximately 40.8% N-glucuronide metabolite, 7.7% other metabolites, and 9% unchanged parent drug, while virtually the entire portion recovered in the feces comprised unchanged vericiguat.
[A227478]
[L31153][A227478]
Proteins and enzymes this drug interacts with in the body
PMID:15123990 PMID:21928830 PMID:26100624 PMID:30319355 PMID:9600905
May also participate in the trafficking of membrane-asociated proteins to the photoreceptor outer segment membrane (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC C01DX22
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Vericiguat
Additional database identifiers
Drugs Product Database (DPD)
23829
ChemSpider
32700337
BindingDB
50239781
ZINC
ZINC000072318626
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4687
GeneCards
GUCY1B1
Guide to Pharmacology
1290
UniProt Accession
GCYB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4689
GeneCards
GUCY2D
UniProt Accession
GUC2D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12541
GeneCards
UGT1A9
GenBank Gene Database
S55985
GenBank Protein Database
7690346
UniProt Accession
UD19_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q27283201), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.