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miconazole + benzoyl peroxide (Acnidazil / Acne Creme Plus)

✓ Approved

Teva Pharmaceutical Industries Ltd. · Small Molecule · Small Molecule

What is miconazole + benzoyl peroxide?

miconazole + benzoyl peroxide is a small molecule developed by Teva Pharmaceutical Industries Ltd.. It is approved for therapeutic indications.

Drug Profile

Brand NamesAcnidazil, Acne Creme Plus
CompanyTeva Pharmaceutical Industries Ltd.
Drug ClassSmall Molecule
StatusApproved
Sources: ClinicalTrials.gov, Teva Pharmaceutical Industries Ltd.

Therapeutic Indications

miconazole + benzoyl peroxide is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersAcne✓ Approved

Related Research Articles

PubMedRSC advances2026-11-12

Hydrogen peroxide-responsive fluorescent probes based on aromatic imidazole derivatives: design, optimization and biomedical applications.

Zhu Yanshuang Y

Hydrogen peroxide (H2O2) is a key bioactive molecule involved in various physiological processes, including cellular signal transduction, oxidative stress regulation, and immune metabolism. Disruption of H2O2 homeostasis is closely associated with the initiation and progression of multiple diseases, particularly tumors. In this study, we leveraged the ultrahigh brightness of aromatic imidazole carbaldehyde derivatives to design a series of novel H2O2-responsive fluorescent probes. By integrating two distinct H2O2-responsive moieties with these highly luminescent fluorophores, we successfully synthesized the probes designated as BTI, BTB, PTI, and PTB, which could be specifically activated by exogenous or endogenous H2O2 in cancer cells. Among these probes, PTI exhibited highest sensitivity and best selectivity toward H2O2 in vitro (LOD = 77 nM), enabling H2O2 mapping in HEp-2 cells and image-guided surgery in mouse models bearing subcutaneous tumors. Meanwhile, upon light irradiation, PTI exhibits efficient reactive oxygen species (ROS) generation and effective suppression of HEp-2 cell viability, positioning it as a promising photosensitizer for photodynamic therapy (PDT) in the treatment of laryngeal squamous cell carcinoma (LSCC).

PMID 43017449
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PubMedPest management science2026-11-12

miR-486-3p knockdown induces testicular ferroptosis by upregulating Acsl4 in mice: a novel molecular target for non-lethal fertility control of rodent pests.

An Kang K, Ou Kejie K, Zhao Zongxi Z, Kang Jia J et al.

Rodent population outbreaks pose serious threats to public health and agricultural production. Traditional lethal rodenticides can cause environmental contamination and poisoning of nontarget organisms, while raising animal welfare concerns, creating an urgent demand for environmentally friendly, nonlethal control strategies. Fertility control through intervention at key molecular targets enables population regulation while preserving ecological integrity, making it a promising nonlethal alternative. Ferroptosis-mediated impairment of testicular function provides a theoretical basis for male fertility control. Nevertheless, key regulatory targets in this pathway remain poorly defined. Here, we used mice as a model to investigate a potential molecular target for inducing male reproductive impairment, laying the foundation for future applications in rodent pest population control. We found that miR-486-3p targets the ferroptosis-associated gene encoding acyl-CoA synthetase long-chain family member 4 (Acsl4) and inhibits its expression. miR-486-3p overexpression alleviated peroxide accumulation induced by RAS selective lethal 3 in Sertoli cells and testicular tissue, reducing sensitivity to ferroptosis and indicating that miR-486-3p plays a critical role in regulating ferroptosis. Local knockdown of miR-486-3p in the testis induced peroxide accumulation and ferroptosis, disrupted the seminiferous tubule structure, and caused a 10.8% reduction in testicular weight and a 78.2% reduction in epididymal sperm count. Our results suggest that miR-486-3p knockdown induces ferroptosis-associated testicular damage by upregulating Acsl4, providing a candidate target for developing nonlethal interventions for rodent pest population management via male fertility control. © 2026 Society of Chemical Industry.

PMID 43015944
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PubMedChemSusChem2026-11-12

Photocatalytic Coproduction of H2 and H2O2: Mechanistic Insights, Material Design, and Challenges in the Two-Electron Water Oxidation Reaction.

Giacchero Arianna A, Ricco Francesco F, Paganini Maria Cristina MC, Naldoni Alberto A

Photocatalytic coproduction of hydrogen (H2) and hydrogen peroxide (H2O2) from pure water via the two-electron water oxidation reaction (2e--WOR) represents a novel approach toward sustainable solar-to-chemical energy conversion. This enables the parallel generation of two high-added-value products, offering a promising alternative to conventional systems. This review summarizes the latest advancements obtained using this approach and heterogeneous semiconductor photocatalysts. After introducing the fundamentals of photocatalysis, the thermodynamics, kinetics and mechanisms of water reduction and oxidation are discussed, accounting for the distinct competing pathways. Energetics and selectivity of H2O2 production are assessed using free-energy descriptors and volcano plot analysis. Stability of H2O2 under photocatalytic conditions is examined, considering thermal, photochemical, and surface-mediated decomposition processes. Material design strategies to promote photocatalytic H2/H2O2 coproduction are critically analyzed and discussed. These include doping, defect engineering, morphology control, cocatalyst integration, and heterojunction formation. The aim of this review is to provide general guidelines for designing new efficient nanomaterials for photocatalytic H2/H2O2 coproduction, minimizing H2O2 degradation. Finally, it offers a critical assessment of reported approaches, providing insights into the current level of progress in this field: the experimental evidence underlying mechanism assignment is examined and organized into a hierarchy, against which the surveyed systems are classified.

PMID 43018123
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PubMedBiophysical reviews2026-11-12

Assessing photodynamic therapy under in vitro hypoxia: photochemical pathways and methodological challenges.

da Cunha Ieda Vieira IV, Caetano Mayara Martins MM, Bessas Naiara Cristina NC, Biazzotto Juliana Cristina JC et al.

Photodynamic therapy (PDT) is a light-activated modality that kills cells through photosensitizer-triggered reactive oxygen species, but its efficacy is strongly shaped by oxygen availability and by whether photochemistry proceeds through Type I or Type II pathways. In oxygen-rich settings, Type II PDT mainly generates singlet oxygen, whereas hypoxia suppresses this route and shifts interest toward Type I mechanisms that produce radical species such as superoxide, hydroxyl radicals, and hydrogen peroxide. This review argues that hypoxia-driven resistance in vitro is not explained by oxygen depletion alone, but by interactions among photochemical pathway choice, cellular adaptation, photosensitizer uptake and localization, and assay limitations. It highlights that hypoxia can reshape membrane composition, vesicular trafficking, and organelle targeting, which in turn alters reactive oxygen species patterns and photodamage outcomes. Methodologically, the work recommends Controlled hypoxia models, including 2D low oxygen cultures and 3D spheroids, together with orthogonal readouts of hypoxia and oxidative damage. For ROS profiling, it supports comparing normoxic and hypoxic conditions using probes for total ROS, superoxide, hydroxyl radicals, and singlet oxygen, because no single assay captures the full mechanistic picture. Finally, it emphasizes that lipid and protein oxidation should be interpreted with caution in hypoxic PDT, since FOX, TBARS, iodometric methods, and BODIPY-C11 mainly report secondary or localized products and may miss Type I driven damage unless combined with imaging, membrane integrity assays, and time-resolved measurements.

PMID 43016941
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PubMedFrontiers in pharmacology2026-11-12

Intracellular glutathione availability, rather than vitamin C supplementation, determines endothelial cell resistance to water-soluble cigarette smoke toxicants.

Oñate Gloria G, Salgado Perla P, Guzmán Paula A PA, Muñoz Alejandra A et al.

Smoking involves chronic exposure to cigarette smoke toxicants, which is associated with the development of vascular disease characterized by endothelial dysfunction. We examined the role of glutathione and vitamin C in antioxidant defense in endothelial cells exposed to water-soluble cigarette smoke toxicants. Exposure to cigarette smoke-conditioned medium decreased cell viability in a concentration and time-dependent manner, with rapid glutathione depletion and recovery. Cells exposed to non-lethal concentrations recovered their glutathione levels in a manner related with enhanced cell survival, and disruption of glutathione metabolism with L-buthionine-(S,R)-sulfoximine (BSO) drastically decreased cellular resistance to cigarette smoke toxicity and increased cell death. These negative effects were augmented in cells treated with graded hydrogen peroxide concentrations following exposure to cigarette smoke-conditioned medium. Intracellular vitamin C did not provide sustained protection against cigarette smoke toxicity and did not enhance glutathione recovery following oxidative challenge. Moreover, exposure to cigarette smoke-conditioned medium failed to affect the transport of reduced (ascorbic acid) or oxidized (dehydroascorbic acid) vitamin C by endothelial cells, regardless of the status of intracellular glutathione or vitamin C. We conclude that glutathione and vitamin C possess overlapping but clearly distinct functions in the response of cells to oxidative challenge. Specifically, in endothelial cells exposed to soluble cigarette smoke toxicants, glutathione was the major determinant against cigarette smoke toxicity.

PMID 43017482
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PubMedACS applied materials & interfaces2026-11-12

A Biomimetic Cell Membrane-Coated Nanoreactor Reshapes ROS Homeostasis and Activates STING Pathway for Synergistic Chemodynamic-Immunotherapy.

Ahmad Waqas W, Ashraf Ghazala G, Sajjad Wasim W, Shams Saira S et al.

The combination of chemodynamic therapy (CDT) and immunotherapy offers a promising therapeutic paradigm for advanced cancer treatment, yet its translation is largely hindered by inadequate intratumoral reactive oxygen species (ROS) production and the lack of a robust link between ROS-induced cytotoxicity and durable immune activation. To address these challenges, we herein engineer a multifunctional biomimetic nanoplatform (ZMGM) by encapsulating Mn2+ and glucose oxidase (GOX) within zeolitic imidazolate framework-8 (ZIF-8), followed by surface functionalization with 4T1 breast cancer cell membranes. This design integrates three synergistic functions: (1) GOX depletes glucose and generates hydrogen peroxide (H2O2) within the acidic tumor microenvironment; (2) the produced H2O2 fuels the Mn2+-mediated Fenton-like reaction to amplify ROS production; and (3) Mn2+ simultaneously serves as a potent stimulator of interferon genes (STING) agonist, triggering type-I interferon responses and promoting dendritic cell maturation. Meanwhile, the homologous cancer cell membrane coating endows ZMGM with specific tumor homing and enhanced tumor localization. Both in vitro and in vivo findings demonstrate that ZMGM not only efficiently eradicates primary tumors but also induces a systemic antitumor immune response, characterized by increased CD8+ T cell infiltration, that effectively suppresses distant metastatic lesions. Notably, the synergistic CDT-STING immunotherapy achieves a primary tumor inhibition rate of 84.22% without obvious systemic toxicity. This work provides a paradigm for rationally designing a single nanoplatform that bridges ROS-mediated cell killing and innate immune activation, offering a promising avenue for combating metastatic triple-negative breast cancer.

PMID 43016149
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