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clotrimazole + betamethasone (Flotiran / Lotrisone / Lotricomb)

✓ Approved

Merck & Co. · NR3C1 · Small Molecule

What is clotrimazole + betamethasone?

clotrimazole + betamethasone is a small molecule developed by Merck & Co.. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesFlotiran, Lotrisone, Lotricomb
CompanyMerck & Co.
Drug ClassSmall Molecule
Molecular TargetNR3C1,
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Merck & Co.

Mechanism of Action

Molecular Targets

clotrimazole + betamethasone acts on 2 molecular targets:

NR3C1nuclear receptor subfamily 3 group C member 1 (GR, GCCR)
sterol demethylase, Candida albicans (ERG11)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

clotrimazole + betamethasone is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsWound infection fungal✓ Approved

Related Research Articles

PubMedBiology open2026-10-16

Genetic disruptions of Hsp90-encoding genes impacted short-term evolutionary trajectories of antifungal resistance in Saccharomyces cerevisiae.

Li 李雪莹 Xueying C XC, Liang 梁淼 Miao M, Han 韩欣颖 Xinying X, Li 李万杰 Wanjie W et al.

Laboratory evolution has been a powerful approach to address questions about evolvability. It has been debated whether the molecular chaperone, heat shock protein 90 (Hsp90), buffers or potentiates the effects of variation, and, consequently, constrains or accelerates evolution. In this study, we experimentally evolved yeast strains carrying mutant alleles of Hsp90-encoding genes under mild clotrimazole selection. We found that knockout of HSC82, which encodes a constitutively expressed Hsp90 chaperone, led to slower evolution of clotrimazole resistance in the short term. However, all strains generally evolved resistance within seven transfers, regardless of Hsp90 status. Through whole-genome sequencing, we identified genetic changes associated with clotrimazole resistance, including prevalent mitochondrial genome loss, as well as chromosomal duplications and point mutations. HSC82 knockout populations specifically showed convergent chromosomal duplications of chrVIII and chrXV. Taken together, our results demonstrate that disruption of Hsp90 in yeast may not alter the overall outcome of evolution but may shape its evolutionary trajectories at both the phenotypic and genotypic levels.

PMID 42885508
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PubMedCureus2026-10-15

Disciform Keratitis That Improves With Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor Treatment for Ovarian Cancer but Recurs Upon Discontinuation of Treatment.

Fukushima Atsuki A, Kohno Shintaro S, Tabuchi Hitoshi H

The patient was a 73-year-old woman. She underwent surgery for ovarian cancer but needed chemotherapy because tumor cells were observed at the resection margin. She was administered niraparib tosilate hydrate, a poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, for five years; however, she developed severe malaise that made daily life difficult, rendering continued treatment impossible. Consequently, the PARP inhibitor was discontinued, and her physical condition improved. One year after discontinuation, she developed ocular herpes zoster, followed by disciform keratitis, leading to her presentation at our hospital. Examination of the right eye revealed disciform corneal edema and opacity, resulting in a diagnosis of disciform keratitis. Varicella-zoster virus (VZV) DNA was detected via PCR analysis of the aqueous humor; treatment with oral valacyclovir and topical betamethasone was initiated. Subsequently, the disciform keratitis resolved with continued topical betamethasone therapy. However, ovarian cancer recurrence was observed, and another PARP inhibitor, olaparib, was prescribed. She again experienced malaise, necessitating the discontinuation of the PARP inhibitor. One month after discontinuation, a recurrence of disciform keratitis was observed. Frequent topical betamethasone administration was initiated, resulting in the resolution of the disciform keratitis. These findings suggest the possibility that in patients with cancer who are immunocompromised due to treatment with PARP inhibitors, an immune response against VZV does not occur; however, when immune function recovers upon discontinuation of the PARP inhibitor, the immune response against VZV is reactivated, resulting in the recurrence of disciform keratitis. Thus, when managing patients with cancer, it is essential to monitor fluctuations in immune response while addressing ocular infections and inflammatory diseases.

PMID 42877565
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PubMedJournal of clinical pharmacology2026-10-14

Mechanistic Prediction of Maternal, Fetal, and Amniotic Fluid Betamethasone Concentrations to Support Dosing Optimization in Pregnancy.

Mahdi Alaa A, Abduljalil Khaled K, Moreira Fernanda de Lima FL, Mehta Hiral Raju HR et al.

Respiratory distress syndrome (RDS) remains a major cause of neonatal mortality following premature birth. Antenatal betamethasone is the standard of care to accelerate fetal lung maturation and improve neonatal outcomes; however, current dosing recommendations assume uniform maternal and fetal exposure across pregnancies. Gestational age (GA)-dependent physiological changes and maternal obesity may alter betamethasone disposition and fetal exposure. This study developed a maternal-fetal physiologically based pharmacokinetic (m-f-PBPK) model to quantify the effects of GA and maternal obesity on betamethasone exposure and evaluate current dosing recommendations between 24 and 34 gestational weeks. The m-f-PBPK model incorporated maternal CYP3A-mediated metabolism, placental passive diffusion and active efflux via P-glycoprotein (P-gp), placental metabolic clearance, GA-dependent physiology, and formulation-specific release rates of betamethasone phosphate and acetate. Model performance was evaluated using maternal and fetal exposure metrics across gestation. At GA 30 weeks in non-obese pregnancies, placental metabolic clearance contributed approximately 17% of maternal clearance, whereas fetal hepatic metabolism accounted for only 2.4%. Maternal obesity decreased maternal and fetal exposure by approximately 9%, while morbid obesity reduced exposure by 23%. Simulated fetal concentrations remained above the proposed pre-clinical-derived surrogate marker of 2 ng/mL for a median duration of 38-40 h in non-obese, 37.5-39 h in obese, and 30-32 h in morbidly obese populations. This m-f-PBPK model successfully characterized maternal-fetal pharmacokinetics and provides a mechanistic basis for understanding betamethasone fetal exposure across GAs with and without maternal obesity, supporting optimization of antenatal corticosteroid therapy.

PMID 42872351
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PubMedFrontiers in pharmacology2026-10-14

Knowledge graph and machine learning-guided virtual screening prioritizes putative blockers of the PSMD11/Rpn6-EBOV glycoprotein interface.

Wang Yanshuang Y, Li Yuanjian Y, Zhu Lin L, Jiang Zhiguo Z et al.

Host-directed antiviral discovery requires a traceable route from host-factor identification to testable molecular hypotheses. This study developed such a workflow around a host factor associated with Ebola virus glycoprotein (EBOV GP). GFP-GP pulldown coupled with co-immunoprecipitation/mass spectrometry was used to identify GP-associated host candidates. A PSMD11/Rpn6-centred workflow integrated knowledge-graph inference, ligand-only machine learning, ADMETlab profiling and interface-guided docking. Candidate prioritization was assessed through score-weight sensitivity analysis, applicability-domain assessment and docking controls addressing seed reproducibility, search convergence, whole-receptor context and macrocycle ring-conformer sensitivity. Docking scores were contextualized against a matched 59-compound library. The analysis recovered 424 GP-pulldown-specific host proteins and nominated PSMD11/Rpn6 as a proteostasis anchor. The tier-gated knowledge-graph candidate membership was invariant across the tested weight perturbations, with Spearman rho = 0.998 under equal weighting. The selected ExtraTrees model achieved an AUC of 0.912 for the Ki endpoint. Applicability-domain assessment and ADMET profiling differentiated candidate confidence and predicted liabilities. Docking reproducibility checks yielded a maximum standard deviation of 0.05 kcal/mol for conformationally restricted ligands, while macrocyclic candidates showed greater protocol-dependent variability. Rule-based triage integrating upstream evidence, ADMET burden, chemotype diversity and mechanistic coverage returned five candidates: betamethasone, bafilomycin A1, everolimus, pitavastatin and CHEMBL1410015. The workflow links a proteomic host-factor signal to a compact set of chemically diverse hypotheses with explicit evidence sources and limitations. The candidates remain hypotheses for experimental assessment; direct target engagement, interface blockade and antiviral activity are not established by the present study.

PMID 42870962
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PubMedClinical case reports2026-10-13

Deep Gluteal Syndrome and Persistent Sciatica in a Patient With Unilateral Piriformis Muscle Hypertrophy: A Case Report.

Ghani Najoua N

A man of 47 had 6 months of left sciatica without root compression on lumbar imaging. Pelvic CT showed isolated left piriformis hypertrophy, 700 versus 450 mm2. Guided betamethasone injection relieved him within 48 h, sustained at 6 months. Asymmetry and response support, but do not prove, sciatic nerve entrapment.

PMID 42865704
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PubMedOperative neurosurgery (Hagerstown, Md.)2026-10-12

Predictors of Insufficient Awakening During Awake Surgery: A Single-Center Retrospective Study.

Takada Shigeki S, Hattori Etsuko Yamamoto EY, Ikeda Hiroyuki H, Sano Noritaka N et al.

Awake surgery (AS) is widely performed for the resection of brain tumors and for epilepsy surgery. However, a non-negligible proportion of patients experience insufficient intraoperative awakening, leading to inadequate neurological monitoring. This retrospective study investigated predictive factors associated with insufficient intraoperative awakening. We retrospectively reviewed 78 consecutive AS procedures for brain tumors and epilepsy performed at our institution between 2021 and 2024. Previously reported predictive factors for AS failure and contraindications for AS were evaluated, along with the presence of basal ganglionic involvement (BGI), defined as a high-intensity area on fluid-attenuated inversion recovery imaging involving the striatum and globus pallidus. Insufficient intraoperative awakening occurred in 13 cases (16.7%). Age (odds ratio [OR] per year, 1.04; 95% CI, 1.00-1.08), aphasia (OR, 4.18; 95% CI, 1.23-15.5), midline shift (OR, 7.85; 95% CI, 2.22-30.6), and BGI (OR, 118; 95% CI, 18.7-2352.2) were identified as factors associated with insufficient awakening using univariate logistic regression analysis. In multivariate logistic regression analysis, BGI remained independently associated with insufficient awakening (OR, 104.7; 95% CI, 16.4-2098.1). Preoperative corticosteroids were administered to 11 patients with glioblastoma to reduce peritumoral edema. Among 7 patients with glioblastoma and BGI at admission, BGI resolved preoperatively in 2 patients after corticosteroid therapy, and AS was successfully performed in both cases. Betamethasone was predominantly used, at a median dose of 4 mg/day and median preoperative treatment duration of 14 days. In both cases with resolved BGI, betamethasone was administered at 8 mg/day for more than 10 days. BGI may be one of the independent predictors of insufficient intraoperative awakening across a broader AS population. Preoperative administration of an adequate course of betamethasone may facilitate sufficient intraoperative awakening in patients with glioblastoma and BGI. Further multicenter studies are warranted.

PMID 42861972
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