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betamethasone dipropionate (DFD01 / DFD 01 / Sernivo)

✓ Approved

Encore Dermatology, Inc. · 类固醇 · 类固醇

什么是 betamethasone dipropionate？

betamethasone dipropionate 是一种类固醇，由Encore Dermatology, Inc.研发。该药已获批，用于治疗相关适应症，给药途径：Topical。

药物档案

商品名DFD01, DFD 01, Sernivo
公司Encore Dermatology, Inc.
药物类别类固醇, 小分子
给药途径Topical
状态Approved
来源： ClinicalTrials.gov, Encore Dermatology, Inc.

治疗适应症

betamethasone dipropionate 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Skin and subcutaneous tissue disordersPsoriasis✓ Approved

相关研究文献

PubMedFrontiers in veterinary science2026-09-10

Synergistic in-vitro activity of Fosinopril alone and in combination with imidocarb dipropionate against Babesia bovis.

Bhowmick Biswajit B, Lacy Paul A PA, Suarez Carlos E CE, Chung Chungwon J CJ

Bovine babesiosis, caused by Babesia bovis is a major cattle disease worldwide, particularly in tropical and subtropical regions. A commonly used drug for the control and treatment of babesiosis is imidocarb dipropionate (ID), which has proved effective against B. bovis. Nevertheless, its toxicity to ruminants and other mammals, along with the persistence of drug residues in meat and milk for several months after treatment, has led to restriction on its use. Furthermore, several reports indicate that complete parasite elimination is not obtained in some cases. Interestingly, the angiotensin-converting enzyme (ACE) inhibitor Fosinopril has been recently found to exhibit potent antibabesial activity against Babesia duncani. In this study, we investigated the in-vitro activity of Fosinopril alone and in fixed-ratio combinations with ID against the B. bovis Texas T2Bo isolate. Quantitative dose-response analyses of the in-vitro activity showed that Fosinopril exhibited measurable activity against the Babesia bovis T2Bo isolate, with an IC50 value of 541.2 nM, whereas ID demonstrated greater potency, with an IC50 value of 124.3 nM. When fixed-ratio combination studies were conducted to evaluate interactions between two drugs, the low-dose regimen Comb-4 (108 nM Fosinopril + 25 nM ID) was the only tested combination that met the predefined ΣFIC criterion for synergy (ΣFIC = 0.40). MDBK cells viability testing showed that ID reduced cell viability at the parasite-relevant concentration tested, whereas Fosinopril and the low-dose combination treatments maintained high MDBK cell viability under the same in-vitro screening conditions. Overall, these proof-of-concept in-vitro findings suggest that Fosinopril has potential as a repurposed therapeutic agent for the treatment of B. bovis-infection in cattle. Low-dose Fosinopril-ID combinations may provide a dose-sparing direction for future pharmacological studies.

PMID 42718422
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PubMedJournal of orthopaedic case reports2026-09-09

Clinical Outcomes of Clinico-radiologically Predetermined Patient Specific Multi-site Steroid Injection in Primary Frozen Shoulder: A Prospective Case Series.

Patel Vraj V, Rampurwala Aliasgar A, Joshi Dhwanil D, Shah Stavan S et al.

Frozen shoulder (FS) is characterized by shoulder pain and progressive restriction of the range of motion, for which treatment is aimed at pain relief, improving shoulder function and shortening the course of the condition. Consensus does indeed lean significantly toward conservative management, but choosing the best non-surgical modality can be overwhelming with regards to the myriads of options available and the lack of homogeneity in the literature, which precludes comparability. This led us to design the present case series. Clinico-radiologically predetermined intra-articular and landmark-based multisite betamethasone injection technique yields satisfactory pain relief and improves range of motion (ROM) and clinical outcomes in FS. Patients clinically diagnosed as having primary FS, confirmed by an ultrasound and X-ray of the affected shoulder, were included in the study over a span of 3 years (n - 94). During clinical examination, joint line and bursae were palpated for tenderness. The steroid preparation consisted of 8 mg of betamethasone (4 mg/mL vial) diluted with 8 mL of 2% plain lignocaine. 5 mL of this steroid preparation was injected intra-articularly and the remaining divided among the areas of tenderness and inflammation pre-determined clinically or radiologically by ultrasound. The injections were administered by a single shoulder surgeon, after which physiotherapy was performed for 8 weeks. Follow-up was done at 2, 4, and 8 weeks, during which ROM, Visual Analog Scale (VAS), American Shoulder and Elbow Scoring System (ASES) and Shoulder Pain and Disability Index (SPADI) were evaluated. Statistically significant differences in pre-injection and post-injection values for the following parameters were noted: Mean abduction, forward flexion and external rotation improved from 124 to 167 degrees (P = 0.001), from 123 to 169 degrees (P = 0.040) and from 26 to 50 degrees (P = 0.009), respectively. The mean ASES score improved from 28.8 to 88.9 (P = 0.001), the mean VAS score decreased from 6.7 to 0.7, while the mean internal rotation improved by 3.5 vertebral levels during the same timelines. The results of our study demonstrate that intra-articular combined with clinico-radiologically predetermined patient-specific landmark-based multisite steroid infiltration using betamethasone leads to a remarkable reduction in pain as well as significant improvement in ROM and clinical outcomes in FS.

PMID 42713384
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PubMedNeurobiology of disease2026-09-09

Neuronal monocarboxylate transporter 2 is downregulated and aggravates seizures in a rat model of infantile epileptic spasms.

Liu Jiayu J, Chen Jie J, Lin Haohan H, Wang Duan D et al.

Infantile epileptic spasms syndrome (IESS) is an age-dependent epileptic encephalopathy of the developing brain, yet its underlying mechanisms remain unclear. Monocarboxylate transporter 2 (MCT2) maintains cerebral metabolic homeostasis via energy substrate transport, but its role in IESS epileptogenesis is unknown. We found that MCT2 was predominantly expressed in neurons and downregulated in IESS patient specimens. In contrast, in human temporal lobe epilepsy (TLE) specimens, MCT2 expression showed no statistically significant difference relative to controls. We observed this downregulation of neuronal MCT2 in an IESS rat model. Transcriptomic analysis 24 h post-spasms revealed enrichment in mitochondrial pathways and oxidative phosphorylation. Consistently, translocase of outer mitochondrial membrane 20 (TOMM20) was markedly downregulated in the cortex of IESS patients and a betamethasone/N-methyl-d-aspartate (NMDA)-induced rat model, which also displayed ultrastructural mitochondrial damage, reactive oxygen species accumulation, and an imbalanced Bax/Bcl-xL ratio. Using adeno-associated virus (AAV)-mediated MCT2 knockdown in neonatal rat somatosensory cortex, reduced MCT2 expression significantly shortened latency to spasm onset, increased spasm frequency, and exacerbated post-spasm TOMM20 loss. These findings indicate that impaired MCT2-mediated transport may compromise mitochondrial function and lower the threshold for spasm generation, a characteristic feature of this infantile-onset epilepsy. Neuronal MCT2 thus represents a promising therapeutic target for IESS.

PMID 42716231
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PubMedHypertension (Dallas, Tex. : 1979)2026-09-09

Revealing Causal Proteomic Signatures of Hypertension: Systematic Insights From Proteome-Wide Mendelian Randomization.

Mao Yukang Y, Jiang Yuer Y, Wu Tingting T, Li Peng P et al.

Hypertension is a major cardiovascular risk factor with an incompletely understood cause. We aimed to unravel its proteomic landscape and investigate potential molecular mechanisms underlying its risk related to modifiable exposures. Leveraging protein quantitative trait loci from 3 biobank-scale studies (deCODE, Fenland, and UKB-PPP [UK Biobank Pharma Proteomics Project]) based on distinct proteomic platforms (SomaScan or Olink), we performed proteome-wide Mendelian randomization to identify and cross-platform validate proteins causally associated with hypertension and blood pressure (BP). Bayesian colocalization was applied to detect shared causal variants underpinning the identified associations. A broad range of modifiable risk factors were systematically assessed for their causal associations with hypertension/BP, followed by mediation analyses exploring potential proteomic pathways linking risk factors to hypertension/BP. The discovery Mendelian randomization analyses (deCODE) identified 190 significant causal associations between 118 proteins and hypertension/BP, which were overall consistent in the cross-platform replication analyses (Fenland and UKB-PPP). Fifty-four protein-hypertension/BP pairs were further supported by genetic colocalization. Triangulation of evidence from Mendelian randomization and colocalization prioritized 28 proteins as key causal signatures. Among these, 10 proteins (particularly ALDH2 [mitochondrial aldehyde dehydrogenase] and ULK3 [serine/threonine-protein kinase]) were found to mediate the associations of 8 genetically predicted modifiable risk factors with hypertension/BP, with ALDH2 emerging as a central hub across multiple causal pathways. This study systematically characterized the causal proteomic landscape of hypertension and highlighted proteins implicated in its modifiable risk. These findings provide novel insights into the molecular cause of hypertension and identify promising candidates for further therapeutic investigation.

PMID 42713651
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PubMedInternational journal of pharmaceutics2026-09-08

In vitro evaluation of water-insoluble silicates and polyvinylpyrrolidone-vinyl acetate as oral carriers for amorphous ritonavir: dissolution enhancement and the role of phosphatidylcholine.

Dhumal Gaurav G, Savoy Adélaïde A, Kuentz Martin M, Polli James E JE

Porous silicates have been investigated as drug carriers to promote the solubility and in vitro dissolution of poorly water-soluble drugs, owing to their potential to adsorb drug molecules in the amorphous form within their structural cavities. This study aimed to evaluate the efficiency of bentonite (BT), Aeroperl 300 Pharma (AP), and Florite PS-200 (FR) as water-insoluble silicate drug carriers, and the polymer polyvinylpyrrolidone-vinyl acetate (PVPVA) in improving the dissolution of ritonavir (RTV). The effect of phosphatidylcholine (PC) as a water-insoluble excipient on drug dissolution was also investigated. Multiple linear regression analysis of the dissolution data was performed to identify the factors influencing dissolution, complemented by mechanistic simulations of the best-performing carrier. The in vitro dissolution rank order of carriers with a 30% drug load (DL) based on % dissolved300min was AP = FR > PVPVA = BT in the absence of PC, and AP > FR > PVPVA > BT with PC. The extent of dissolution for all formulations increased in the presence of PC, with the AP and FR formulations exceeding that of marketed formulations. High drug load did not significantly affect the dissolution profile of silicate formulations, but it reduced dissolution from PVPVA solid dispersion. In silico results showed that silicate pore size governed RTV release, with open pores forming fewer hydrogen bonds, allowing more facile RTV release. The significant improvement in RTV dissolution with AP and FR supports the use of these carriers for poorly soluble drugs as alternatives to traditional polymers, especially for formulations with high drug loads.

PMID 42710749
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PubMedCurrent medicinal chemistry2026-09-08

Identification of Causal Plasma Proteins and Immune Mediators for Lung Cancer in Never-Smokers: A Large-Scale Integrative Analysis Combining Mendelian Randomization, Colocalization, and Mediation.

Wu Jian-Cong JC, Zhang Qi Q, Lin Yan-Ming YM, Chen Xiao-Rao XR et al.

As global smoking rates decline, Lung Cancer in Never-Smokers (LCINS) has emerged as a distinct and increasingly important clinical entity. However, its underlying pathogenesis remains poorly understood, highlighting the need to identify circulating molecular determinants and candidate biomarkers. Genetic instruments for plasma proteins were obtained from pQTL datasets (Fenland study and UK Biobank Pharma Proteomics Project), while summary statistics for LCINS were sourced from TRICL-ILCCO. Two-sample Mendelian Randomization (MR) was performed using inverse-variance weighting as the primary approach, complemented by sensitivity analyses for heterogeneity (Cochran's Q), horizontal pleiotropy (MR-Egger intercept), and outlier detection (MR-PRESSO). Tissue-level validation was conducted using CPTAC proteomic data. Further analyses, including Bayesian colocalization, Protein-Protein Interaction (PPI) network construction, Gene Ontology (GO) enrichment, and mediation analysis, were applied to investigate shared genetic architecture, functional pathways, and immune-mediated mechanisms. Among 543 cis-acting plasma proteins evaluated in the discovery phase, 35 exhibited evidence of association with LCINS risk, including 15 positively and 20 inversely associated proteins. After False Discovery Rate (FDR) correction, only genetically proxied plasma RARRES1 remained statistically significant (OR = 1.17, adjusted P = 2.72 × 10-5), and this finding was replicated in an independent cohort. Bayesian colocalization supported a shared causal variant (PPH4 = 0.83). Functional enrichment analyses implicated RARRES1-related networks in immune regulation and extracellular processes. Two-step MR mediation analysis nominated CD16-CD56 intensity on NKT cells as a potential immune-mediated pathway, accounting for an estimated 11.8% of the genetic effect. This study prioritizes genetically proxied plasma RARRES1 as a candidate protein associated with LCINS risk and highlights CD16-CD56 intensity on NKT cells as a potential immune-related mechanism. These findings provide biologically plausible evidence supporting a role for RARRES1 in LCINS pathogenesis and its potential utility in biomarker development. Genetically proxied plasma RARRES1 is associated with increased LCINS risk and may contribute to disease susceptibility through immune-related alterations involving NKT-cell phenotypes. RARRES1 represents a promising candidate for future mechanistic studies and blood-based diagnostic biomarker development in LCINS.

PMID 42708309
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