Drug Database
BE

betamethasone dipropionate (DFD01 / DFD 01 / Sernivo)

✓ Approved

Encore Dermatology, Inc. · Steroids · Steroids

What is betamethasone dipropionate?

betamethasone dipropionate is a steroids developed by Encore Dermatology, Inc.. It is approved for therapeutic indications via topical.

Drug Profile

Brand NamesDFD01, DFD 01, Sernivo
CompanyEncore Dermatology, Inc.
Drug ClassSteroids, Small Molecule
RouteTopical
StatusApproved
Sources: ClinicalTrials.gov, Encore Dermatology, Inc.

Therapeutic Indications

betamethasone dipropionate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersPsoriasis✓ Approved

Related Research Articles

PubMedLasers in medical science2026-07-16

Combined compound betamethasone and 595 nm pulsed dye laser improves hypertrophic scar and is associated with enhanced autophagy in myofibroblasts.

Sui Shijia S, Bian Shijun S, Xia Zhikuan Z, Wu Jiamin J et al.

Compound betamethasone combined with 595 nm pulsed dye laser (PDL) is widely used in the clinical management of hypertrophic scars. However, the mechanisms underlying this enhanced effect remain poorly understood. This study evaluated its therapeutic efficacy and investigated whether induction of autophagy in myofibroblasts is associated with scar improvement. A rabbit ear hypertrophic scar model was established and divided into control, compound betamethasone injection (BI), PDL, and combined (BI + PDL) groups. Scar morphology and histological changes were assessed. Autophagy was evaluated using transmission electron microscopy (TEM) and immunohistochemical detection of LC3B and p62. In vitro, hypertrophic scar-derived myofibroblasts were treated with betamethasone dipropionate (BD), PDL, or their combination (BD + PDL). Cell viability, collagen expression, and autophagic activity were analyzed using CCK-8 assays, Western blotting, MDC staining, immunofluorescence, and TEM. Chloroquine was used to assess autophagic flux. The combined BI + PDL treatment produced the most pronounced improvement in scar architecture, with reduced collagen deposition, decreased microvessel density, and increased number of apoptotic cells. Autophagy levels were significantly elevated in the combination group both in vivo and in vitro. In cultured myofibroblasts, BD + PDL markedly inhibited cell viability and reduced type I and type III collagen expression. This effect was accompanied by increased autophagosome formation, an elevated LC3II/LC3I ratio, and decreased p62 expression. Importantly, inhibition of autophagic flux with chloroquine attenuated the collagen-suppressive effect of the combined treatment. Compound betamethasone combined with 595 nm PDL significantly improves hypertrophic scars, an effect associated with enhanced autophagic activity in myofibroblasts which may partly mediate collagen degradation.

PMID 42461415
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PubMedJournal of aerosol medicine and pulmonary drug delivery2026-07-16

Toward Next-Generation Propellants: Assessing Lung Deposition of Beclometasone Dipropionate, Formoterol, and Glycopyrrolate Formulated with HFA-152a Using Functional Respiratory Imaging.

Matturro Angelo A, Monshi Tousi Navid N, Sadafi Hosein H, Cuoghi Erika E et al.

Pressurized metered-dose inhalers (pMDIs) rely on hydrofluoroalkane (HFA) propellants that have a high global warming potential (GWP). Reformulation with next-generation, low-GWP propellants, such as HFA-152a, offers a strategy to reduce climate impact; however, changes in propellant composition can affect aerosol characteristics and potentially alter lung deposition, requiring robust demonstration of therapeutic equivalence. Functional respiratory imaging, combining high-resolution computed tomography and computational fluid dynamics, was used to compare the lung deposition of a fixed triple combination of beclometasone dipropionate, formoterol fumarate, and glycopyrronium bromide (BDP/FF/GB) delivered via a pMDI formulated with either HFA-134a (Reference) or HFA-152a (Test). Ten patients with chronic obstructive pulmonary disease (GOLD stages 2-4) were retrospectively selected. Patient-specific airway geometries, a standardized inhalation profile, and formulation-specific particle size distributions and plume characteristics were applied. Deposition was quantified in the intrathoracic, central + distal, and peripheral lung regions, and the (central + distal)/peripheral ([C + D]/P) deposition ratio was evaluated. Mean intrathoracic deposition was comparable between the Reference and Test formulations, ranging from 45.95% to 46.88% of the delivered dose (DD). Deposition in the central + distal airways accounted for 12% of DD for both formulations, whereas peripheral deposition predominated, with 33.7% of DD for the Test formulation and 34.5% of DD for the Reference formulation. The (C + D)/P ratios were similar across all active components (0.35-0.37), indicating consistent preferential deposition in the peripheral/small airways. Although inter-patient variability was observed, intra-subject comparisons showed close agreement between propellants. Reformulation of the BDP/FF/GB pMDI with the low-GWP propellant HFA-152a preserved total and regional lung deposition characteristics relative to the current HFA-134a formulation. These findings support the maintenance of deposition performance while enabling a substantial reduction in environmental impact, reinforcing the potential of HFA-152a as a next-generation propellant for carbon minimal pMDI therapies.

PMID 42461266
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PubMedObstetrics and gynecology2026-07-16

Child Neurodevelopmental Outcomes After Late Preterm Hypoglycemia.

Gyamfi-Bannerman Cynthia C, de Voest Jessica A JA, Tita Alan T N ATN, Blackwell Sean C SC et al.

To evaluate whether hypoglycemia in neonates born to mothers at risk for late preterm delivery was related to adverse effects on childhood neurodevelopment. This was a prospective follow-up study of children aged 6 years or older whose mothers were enrolled in the Antenatal Late Preterm Steroids multicenter randomized trial. The study was conducted at 13 centers that participated in the Maternal-Fetal Medicine Units Network cycle from 2011 to 2016. Follow-up was from 2017 to 2022. Adult consent and child assent were obtained. The primary exposure was hypoglycemia , defined as a blood glucose concentration less than 40 mg/dL within 24 hours of birth. The primary outcome, proportion of GCA (General Conceptual Ability) scores lower than 85 (-1 SD) from the DAS-II (Differential Ability Scales, 2nd Edition), was analyzed by the presence of hypoglycemia at birth, irrespective of initial trial treatment assignment (betamethasone or placebo). Secondary outcomes included GMFCS (Gross Motor Function Classification System) level, SRS-2 (Social Responsiveness Scale, 2 nd Edition) scores, and CBCL (Child Behavior Checklist) scores. Univariable and multivariable analyses were performed, the latter adjusted for prespecified variables known to be associated with the primary outcome. Of 1,026 children enrolled, 1,020 (99.4%) had blood glucose data and 944 had data for the primary outcome. Of these 944, 785 (83.2%) were delivered late preterm and 208 (22.0%) had hypoglycemia, of whom 84 (40.4%) were treated. Those with hypoglycemia were more likely to have private insurance, have older mothers, receive betamethasone, and identify as White. There were no differences in the primary outcome, GCA score lower than 85 (15.9% in those with hypoglycemia vs 18.5% in those without; adjusted relative risk 1.03; 95% CI, 0.74-1.45), and no difference in secondary outcomes. Severity of hypoglycemia also was not associated with any outcomes. In our cohort, hypoglycemia was not associated with neurodevelopmental outcomes in children born predominantly late preterm.

PMID 42462244
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PubMedCurrent medical research and opinion2026-07-16

Cross-publisher agreement on the defining principles of plain language summaries of publications (PLSPs).

Nobes Sophie S, Soldavin Kelly K, Jenkins Rachel R, McDougall Hamish H et al.

Introduced in 2020, plain language summaries of publications (PLSPs) are standalone articles that aim to expand the reach of scientific findings to non-specialist audiences using plain language and meaningful visuals. Despite increased publication, there is no agreed cross-publisher definition of PLSPs, resulting in inconsistent terminology, formatting, peer-review processes, and metadata that hinder indexing and discoverability in bibliographic databases such as PubMed and Europe PMC. In February 2024, the multistakeholder collaboration Open Pharma launched an initiative to review existing standards and practices related to the publication of PLSPs. After identifying three publishers offering standalone PLSPs - Becaris Publishing, Sage, and Taylor & Francis - representatives from each formed a steering committee to define PLSPs and agree on principles that differentiate them from other publishing formats. PLSPs are defined as standalone summaries of peer-reviewed articles, written according to plain language principles, published open access with a unique digital object identifier (DOI), and are themselves peer reviewed (including by someone who is not a scientific specialist in the topic area). They should include a summary, clear reference to the original article, and a combination of text and meaningful graphics. This consensus provides a foundation for standardizing PLSPs as a distinct article type and acceptable secondary publication format. We hope it will also support consistent authoring, editorial management, peer-review processes and indexing. We call on indexing services to formally recognize PLSPs and on publishers to adopt this format as an accurate and reliable source of understandable scientific information.

PMID 42459035
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PubMedTopics in companion animal medicine2026-07-15

Concurrent Babesia gibsoni infection as a negative prognostics indicator of survival in dogs diagnosed with immune-mediated hemolytic anemia: A prospective cohort study.

Bandaranayaka Nishadi N, Dissanayake Anuruddhika A, Jinadasa Rasika R, Govinna Mihidum M et al.

Immune-mediated haemolytic anaemia (IMHA) is a common autoimmune disorder in dogs. Haemoparasites, particularly intracellular organisms, are well-recognized causes of secondary IMHA and are associated with poorer clinical outcomes. However, the prognostic impact of concurrent Babesia gibsoni infection in dogs with IMHA remains incompletely characterized. This study aimed to compare survival outcomes between dogs with primary IMHA and those with IMHA associated with B. gibsoni infection. Fifty-five dogs (34 purebred, 21 crossbred; age 7 months-9 years) diagnosed with IMHA, according to ACVIM guidelines, were included. Twenty-six dogs had primary IMHA (11 males, 15 females), and 29 dogs had IMHA with natural B. gibsoni infection (12 males, 17 females), confirmed by PCR. All dogs received immunosuppressive therapy consisting of prednisolone (1 mg/kg q12h PO) or dexamethasone sodium phosphate (0.2 mg/kg q24h IV). Dogs with B. gibsoni infection additionally received antibabesial treatment that included initial imidocarb dipropionate (6.6 mg/kg IM) in two weeks interval, and doxycycline up to three weeks (10 mg/kg q12h PO). Cases were followed for 60 days. Survival analysis was performed using Cox proportional hazards regression. During follow-up, 40 dogs died of IMHA and 2 from unrelated causes. In multivariable analysis, male sex (HR=2.1; 95% CI: 1.1-4.2; p=0.034), marked spherocytosis (HR=2.1; 95% CI: 1.1-4.3; p=0.032), and concurrent B. gibsoni infection (HR=2.6; 95% CI: 1.2-2.9; p=0.024) were independently associated with increased hazard of death. In conclusion, male sex, marked spherocytosis, and B. gibsoni co-infection are key independent predictors of a poor prognosis in dogs with IMHA.

PMID 42448039
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PubMedJournal of inflammation research2026-07-15

Genetically Predicted Associations of CX3CL1 and UMOD with Acute Kidney Injury Risk: Evidence from Mendelian Randomization and Clinical Validation.

Yang Liu L, Xu Yan Y, Liang Yan Y, Lan Chao C et al.

Acute kidney injury (AKI) is a common clinical syndrome with poor prognosis and limited targeted therapies. This study aimed to systematically identify genetically supported candidate proteins associated with AKI and to explore potential biological pathways and phenotypic associations. Using data from the UK Biobank Pharma Proteomics Project (UKB-PPP), FinnGen, IEU Open GWAS, and other large-scale databases, we applied summary-data Mendelian randomization (SMR), Bayesian colocalization analysis, two-sample Mendelian randomization (MR), mediation analysis, and phenome-wide association study (PheWAS) to assess the causal relationships and mechanisms linking plasma proteins to AKI risk.We collected blood samples undergoing cardiac surgery with cardiopulmonary bypass to measure the levels of CX3CL1 and UMOD in the plasma and compare them with indicators such as serum creatinine and urinary [TIMP2]*[IGFBP7], to evaluate the efficacy of CX3CL1 and UMOD in diagnosing AKI. Two plasma proteins, CX3CL1 and uromodulin (UMOD), were identified as significantly and positively causally associated with AKI risk, supported by genetic colocalization evidence. Mediation analysis indicated that CX3CL1's effect on AKI may be partially mediated by metabolites such as 1,6-anhydroglucose and Mannitol. PheWAS revealed associations of these proteins with hypertension, carbohydrate metabolism disorders, and infections, suggesting potential off-target effects that should be considered in drug development. The associations of these two proteins were further evaluated in human plasma samples.we found that patients with I/R-induced AKI exhibited significantly elevated plasma levels of CX3CL1 and UMOD compared to those who underwent ischemia-reperfusion without developing AKI (P< 0.05). Spearman's test demonstrated a significant correlation between serum creatinine and plasma CX3CL1 and UMOD in patients with I/R induced AKI (r = 0.848, P < 0.001; r = 0.794, P< 0.001, respectively). Plasma CX3CL1 and UMOD showed high specificity but low sensitivity in diagnosing AKI (sensitivity 68.0% and 60%;specificity 92.0% and 88%,respectively). This study systematically elucidates the genetic evidence and possible pathogenic mechanisms of CX3CL1 and UMOD as candidate proteins for AKI, CX3CL1 and UMOD demonstrated potential associations with I/R-induced AKI risk in the present cohort., enriching our understanding of AKI pathogenesis and providing theoretical and safety considerations for future targeted drug development.

PMID 42454155
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