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ID

idoxuridine (Virexen 40% / idoxuridine, Vinas)

✓ Approved

Vinas · · Small Molecule

What is idoxuridine?

idoxuridine is a small molecule developed by Vinas. It is approved for therapeutic indications via topical.

Drug Profile

Brand NamesVirexen 40%, idoxuridine, Vinas
CompanyVinas
Drug ClassSmall Molecule
Molecular Target,
RouteTopical
StatusApproved
Sources: ClinicalTrials.gov, Vinas

Mechanism of Action

Molecular Targets

idoxuridine acts on 2 molecular targets:

(UL30)
(UL30)
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Therapeutic Indications

idoxuridine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsHerpes virus infection✓ Approved

Related Research Articles

PubMedPLoS pathogens2026-01-26

Anti-orthopoxvirus drugs inhibit lumpy skin disease virus replication by targeting viral DNA polymerase.

Gong Zuxin Z, Dai Jiaqi J, Qu Hailong H, Hu Yongxin Y et al.

Lumpy skin disease (LSD) is an emerging transboundary disease caused by lumpy skin disease virus (LSDV), posing significant threats to global cattle health in the absence of validated drugs. Here, we constructed a recombinant LSDV (rLSDV) expressing both mCherry and luciferase reporters for high-throughput drug screening, and the rLSDV retained virological characteristics phenotypically indistinguishable from the parental strain, with the reporter genes serving as precise and sensitive quantitative indicators for viral replication. Leveraging this platform, we identified six candidates from a library of anti-orthopoxvirus compounds, namely cytarabine (AraC), enrofloxacin (ENR), idoxuridine (IDU), fialuridine (FIAU), ribavirin (RBV), and vidarabine (AraA), demonstrating high antiviral activity concomitant with low cytotoxicity. Time-of-addition experiments revealed that all identified candidates primarily inhibited the viral replication phase. Mechanistical analysis revealed that anti-LSDV agents suppressed synthesis of both viral and host DNA and/or RNA. In particular, AraC markedly blocked viral DNA synthesis and prevented activation of viral late gene promoters, thereby arresting the replication cycle at an early stage. Structural alignment data suggested that AraC may bind to the viral DNA polymerase at residues D554, R639, K666, N670, and D758 to inhibit its activity. Notably, AraC induced only minimal host DNA damage and apoptosis, and host DNA synthesis gradually recovered during treatment, although these residues are conserved in bovine DNA polymerase. Hence, the mechanistic landscape delineated herein, together with the established clinical availability of the anti-orthopoxvirus agents, underscore their potential as repurposable therapeutics for LSDV infection.

PMID 41587213
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PubMedInternational journal of biological macromolecules2025-10-13

One-pot enzyme cascade production of therapeutic deoxyribonucleoside analogs from glycerol and acetaldehyde.

Lee Ja Hyun JH, Kim Yoonjoo Y, Kim Dong Hyun DH, Kim Kyoung Heon KH

In this study, we demonstrated a novel one-pot enzyme cascade for the production of deoxyribonucleoside analogs using glycerol and acetaldehyde (AcH) as feedstocks. In the initial stage of the cascade, 2-deoxy-D-ribose 5-phosphate (D-dRib 5P) was generated in situ from glycerol via a non-hydrolytic aldol addition between D-glyceraldehyde 3-phosphate (D-GAP) and AcH, catalyzed by aldolase. D-dRib 5P was subsequently converted into target deoxyribonucleosides through a retrosynthetic enzyme cascade that effectively reverses the natural deoxyribonucleoside salvage pathway, with the choice of nucleobases and nucleoside phosphorylases determining the final products. A key limitation-yield reduction due to the accumulation of free hydrogen phosphate (HPO₄2-)-was strategically addressed by modulating HPO₄2- levels through a free HPO₄2--scavenging system employing sucrose phosphorylase and excess sucrose. Using this approach, we successfully synthesized four commercially relevant therapeutic deoxyribonucleosides-floxuridine, idoxuridine, decitabine, and cladribine-by varying the nucleobases and nucleoside phosphorylases. These findings highlight the potential of this biocatalytic platform for the sustainable and cost-effective production of deoxyribonucleoside analogs from simple, renewable feedstocks.

PMID 41077202
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PubMedVeterinary ophthalmology2025-08-31

Canine Herpesvirus-1 Ocular Infection in Japan: A Case Report.

Usami Kensuke K, Komatsu Hiroyuki H, Akasaka Minori M, Morita Maresuke M et al.

To describe the clinical manifestations and therapeutic outcomes of ocular infection caused by canine herpesvirus 1 (CHV-1), including both typical and atypical features. A client-owned 5-year-old castrated male French Bulldog presented with dendritic corneal ulcers, quantitative tear deficiency, and corneal hypoesthesia in the left eye. A diagnosis of CHV-1 ocular infection was made based on the characteristic presentation of dendritic corneal ulcers and confirmed by polymerase chain reaction (PCR) analysis of a conjunctival swab. Antiviral therapy with 0.1% idoxuridine ophthalmic solution was initiated on Day 8, and follow-up ophthalmic examinations were performed on Days 14, 37, and 58. To monitor viral shedding, conjunctival swabs were collected before and after the initiation of antiviral treatment and analyzed using the quantitative PCR method. Resolution of the corneal ulcers, along with improvement in corneal sensitivity and tear production, was observed. Quantitative PCR revealed a reduction in viral shedding following treatment. No recurrence of ocular lesions was noted by the time of the final follow-up examination. To the authors' knowledge, this is the first documented case of CHV-1 ocular infection in an adult dog in Japan. These findings suggest that CHV-1 may cause not only characteristic corneal ulcers but also associated corneal hypoesthesia and quantitative tear deficiency.

PMID 40886057
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PubMedPloS one2024-11-06

Identification of small molecule agonists of fetal hemoglobin expression for the treatment of sickle cell disease.

Yang Jian-Ping JP, Toughiri Rachel R, Gounder Anshu P AP, Scheibe Dan D et al.

Induction of fetal hemoglobin (HbF) has been shown to be a viable therapeutic approach to treating sickle cell disease and potentially other β-hemoglobinopathies. To identify targets and target-modulating small molecules that enhance HbF expression, we engineered a human umbilical-derived erythroid progenitor reporter cell line (HUDEP2_HBG1_HiBiT) by genetically tagging a HiBiT peptide to the carboxyl (C)-terminus of the endogenous HBG1 gene locus, which codes for γ-globin protein, a component of HbF. Employing this reporter cell line, we performed a chemogenomic screen of approximately 5000 compounds annotated with known targets or mechanisms that have achieved clinical stage or approval by the US Food and Drug Administration (FDA). Among them, 10 compounds were confirmed for their ability to induce HbF in the HUDEP2 cell line. These include several known HbF inducers, such as pomalidomide, lenalidomide, decitabine, idoxuridine, and azacytidine, which validate the translational nature of this screening platform. We identified avadomide, autophinib, triciribine, and R574 as novel HbF inducers from these screens. We orthogonally confirmed HbF induction activities of the top hits in both parental HUDEP2 cells as well as in human primary CD34+ hematopoietic stem and progenitor cells (HSPCs). Further, we demonstrated that pomalidomide and avadomide, but not idoxuridine, induced HbF expression through downregulation of several transcriptional repressors such as BCL11A, ZBTB7A, and IKZF1. These studies demonstrate a robust phenotypic screening workflow that can be applied to large-scale small molecule profiling campaigns for the discovery of targets and pathways, as well as novel therapeutics for sickle cell disease and other β-hemoglobinopathies.

PMID 39504332
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PubMedVirology2024-09-18

5-Bromo-2'-deoxyuridine inhibits African swine fever virus (ASFV) replication via interfering viral DNA replication and suppressing the formation of viral factories.

Long Feixiang F, Ou Weixin W, Liu Zexin Z, Su Guanming G et al.

African swine fever (ASF), caused by ASF virus (ASFV), represents one of the most economically important viral infectious diseases in swine industry worldwide. So far there is no vaccine or antiviral drug for controlling ASF pandemics. In the present study, we assessed inhibition of six nucleoside analogues against ASFV replication in ex vivo primary porcine alveolar macrophages (PAMs), including the first approved antiviral drug idoxuridine. Our results showed that, out of the assessed six compounds, 5-Bromo-2'-Deoxyuridine (5-BrdU, an analog of idoxuridine), exhibited the strongest inhibition on the replication of ASFV in PAMs with a 50% inhibitory concentration (IC50) value of 2.9 μM and a low cytotoxicity (CC50 > 270 μM). Moreover, we showed that 5-BrdU interferes with ASFV DNA replication by incorporating into viral replicating DNA molecules as a competitive substrate for deoxythymidine, ultimately inhibiting the formation of ASFV viral factories. Altogether, our findings suggest that 5-BrdU could serve as a promising therapeutic agent for combating ASFV infection.

PMID 39288610
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PubMedViruses2024-05-25

A Screening Study Identified Decitabine as an Inhibitor of Equid Herpesvirus 4 That Enhances the Innate Antiviral Response.

Normand Camille C, Thieulent Côme J CJ, Fortier Christine C, Sutton Gabrielle G et al.

Equid herpesvirus 4 (EHV-4) is a common respiratory pathogen in horses. It sporadically induces abortion or neonatal death. Although its contribution in neurological disorders is not clearly demonstrated, there is a strong suspicion of its involvement. Despite preventive treatments using vaccines against EHV-1/EHV-4, the resurgence of alpha-EHV infection still constitutes an important threat to the horse industry. Yet very few studies have been conducted on the search for antiviral molecules against EHV-4. A screening of 42 antiviral compounds was performed in vitro on equine fibroblast cells infected with the EHV-4 405/76 reference strain (VR2230). The formation of cytopathic effects was monitored by real-time cell analysis (RTCA), and the viral load was quantified by quantitative PCR. Aciclovir, the most widely used antiviral against alpha-herpesviruses in vivo, does not appear to be effective against EHV-4 in vitro. Potential antiviral activities were confirmed for eight molecules (idoxuridine, vidarabine, pritelivir, cidofovir, valganciclovir, ganciclovir, aphidicolin, and decitabine). Decitabine demonstrates the highest efficacy against EHV-4 in vitro. Transcriptomic analysis revealed the up-regulation of various genes implicated in interferon (IFN) response, suggesting that decitabine triggers the immune antiviral pathway.

PMID 38793627
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