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desloratadine + pseudoephedrine (Clarinex D / Aerinaze)

✓ Approved

Merck & Co. · HRH1 · 小分子

什么是 desloratadine + pseudoephedrine？

desloratadine + pseudoephedrine 是一种小分子，由Merck & Co.研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Clarinex D, Aerinaze
公司Merck & Co.
药物类别小分子
分子靶点HRH1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Merck & Co.

作用机制

分子靶点

desloratadine + pseudoephedrine 作用于 1 个分子靶点：

HRH1histamine receptor H1 (HH1R, H1R)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

desloratadine + pseudoephedrine 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
Immune system disordersSeasonal allergy✓ Approved

相关研究文献

PubMedBMC chemistry2026-10-22

Eco-sustainable organic solvent-free spectrophotometric method for the concurrent determination of a ternary pharmaceutical mixture.

Hamdy Abdallah M AM, Meselhy Esraa M EM, El Henawee Magda M MM, Hashem Hisham H et al.

In recent years, green analytical chemistry has become essential in pharmaceutical research, aiming to mitigate environmental hazards associated with conventional analytical practices. The current focus lies in optimizing analytical methods to achieve both environmental and economic sustainability. In this framework, three environmentally sustainable spectrophotometric methods were developed for simultaneous analysis of three co-formulated drugs: acetaminophen, dextromethorphan hydrobromide, and pseudoephedrine hydrochloride, which are often used to alleviate symptoms associated with COVID-19. The employed spectrophotometric methodologies include the double divisor-ratio spectra derivative method, the mean centering of double divisor ratio spectra method, and the dual wavelength in ratio spectrum method. The innovative techniques displayed good linearity within 25-350 µg/mL for dextromethorphan hydrobromide, 2-24 µg/mL for acetaminophen, and 100-1400 µg/mL for pseudoephedrine hydrochloride. The environmental sustainability of the proposed methods was evaluated using the Analytical Eco-Scale, analytical greenness metric, and the Green Analytical Procedure Index. Furthermore, complementary evaluations of blueness and whiteness were conducted through the Blue Applicability Grade Index and the Red Green Blue 12 metric, respectively. The collective outcomes of all evaluation metrics clearly demonstrated that the proposed methods possess enhanced environmental compatibility and sustainability relative to the existing techniques. The proposed methods were fully validated according to the International Conference on Harmonization recommendations. The developed methods offered a cost-effective and eco-friendly approach for concurrent determination of acetaminophen, dextromethorphan hydrobromide, and pseudoephedrine hydrochloride in their bulk substances, and pharmaceutical formulations.

PMID 42907898
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PubMedSupportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer2026-10-19

Association between prophylactic desloratadine use and docetaxel-induced skin toxicities in patients with early-stage breast cancer: an inverse probability-weighted retrospective cohort study.

Makihara Katsuya K, Kongo Keisuke K, Motomura Kayo K, Kimoto Daiki D et al.

Docetaxel (DTX) causes skin toxicities despite dexamethasone-based supportive care, and no established adjunctive primary prophylaxis exists. We assessed whether desloratadine, a peripheral H1-receptor antagonist with anti-inflammatory properties, was associated with DTX-related skin toxicities in early-stage breast cancer. This single-center retrospective cohort included 143 patients with stage I-III breast cancer receiving perioperative DTX-based chemotherapy (75 mg/m2 every 3 weeks) with dexamethasone premedication. Desloratadine (5 mg daily from the morning after first DTX infusion through treatment completion) was prescribed nonrandomly to 49 patients (34.3%); 94 received no prophylactic antihistamine. The primary outcome was any patient-reported skin toxicity (rash, pruritus, or hand-foot syndrome [HFS]). The primary analysis used Hájek-normalized stabilized inverse probability of treatment weighting (IPTW), with 95% confidence intervals (CIs) from 2,000 patient-level bootstrap resamples with propensity-score refitting. Calendar-time confounding was assessed by post-implementation restriction. After stabilized IPTW, skin-toxicity incidence was 46.2% with desloratadine and 70.7% without it (risk difference, - 24.6 percentage points; 95% CI, - 43.0 to - 5.3; risk ratio [RR], 0.65; 95% CI, 0.42-0.92). Descriptive estimates indicated lower pruritus incidence (RR, 0.36; 95% CI, 0.08-0.79), a lower but imprecise rash estimate (RR, 0.70; 95% CI, 0.43-1.03), and no lower HFS incidence (5.9% vs 5.4%). Post-implementation findings were similar (RR, 0.61; 95% CI, 0.42-0.90); negative-control neuropathy was not lower (RR, 1.19; 95% CI, 0.52-2.58). Desloratadine prophylaxis was associated with lower skin-toxicity risk, particularly for pruritus. Rash risk was lower but imprecisely estimated; HFS risk was not lower. These hypothesis-generating findings warrant validation in a prospective randomized trial.

PMID 42895563
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PubMedThe Journal of allergy and clinical immunology2026-10-16

Comparative efficacy and safety of antihistamines, increased antihistamine dosing, and antihistamine adjuncts for chronic urticaria: a systematic review, dose-response, and network meta-analysis of randomized trials.

Chu Alexandro W L AWL, Zhao Irene X IX, Rayner Daniel G DG, Guyatt Gordon H GH et al.

Chronic urticaria is a common immune-mediated condition characterized by wheals (itch and hives), angioedema, or both, lasting for greater than six weeks. It is managed with H1 antihistamines as the first-line therapy. Fundamental unresolved questions remain regarding the comparative benefits and harms of antihistamines and their adjuncts, and of H1 antihistamine dose-escalation. To analyze the comparative benefits and harms of antihistamines and their adjuncts (H2 blockers or montelukast), and of H1 antihistamine dose-escalation. As part of updating the American Academy of Allergy, Asthma & Immunology and American College of Allergy, Asthma and Immunology Joint Task Force on Practice Parameters Chronic Urticaria guidelines, we searched MEDLINE, EMBASE, CENTRAL, and regulatory databases from inception to March 17, 2025, for randomized trials addressing antihistamines or their adjuncts for chronic urticaria. Paired reviewers independently screened records, extracted data, and assessed risk of bias. Random effects network and dose-response meta-analyses addressed urticaria activity (composed of itch and wheal scores), angioedema activity, urticaria-related quality of life, and harms including sedation. The GRADE approach informed certainty of evidence ratings. CRD42022367280. 211 trials (22,187 participants) evaluated 55 unique treatments. Bilastine, desloratadine, fexofenadine, and levocetirizine are among the most effective in improving overall urticaria activity, urticaria-related quality of life, and sleep disturbance. Cetirizine and loratadine are among the most effective in reducing overall urticaria activity and its subcomponents, with cetirizine also among the most effective in improving urticaria-related quality of life. Escalating from a single to quadruple daily dose may yield diminishing additional benefit. Second-generation agents as a class may be more effective than first-generation agents in improving urticaria activity and sleep disturbance. Sedation risk likely increases with higher doses, with first-generation agents (e.g., diphenhydramine, hydroxyzine) and doxepin among the most sedating; cetirizine, ketotifen, levocetirizine, and rupatadine among the intermediate sedating; and bepotastine, bilastine, desloratadine, ebastine, fexofenadine, and loratadine among the least sedating. Adding montelukast (moderate certainty) or an H2 blocker (very low certainty) to a second-generation agent may further reduce urticaria activity. For chronic urticaria, second-generation agents differ in their efficacy and safety. First-generation agents are less beneficial and more harmful. Escalating to higher daily doses may provide additional benefits but likely increases sedation.

PMID 42887704
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PubMedThe American Journal of dermatopathology2026-10-15

Neutrophilic Fixed Drug Eruption Mimicking Neutrophilic Dermatosis: Two Cases, Including Sequential Biopsies Demonstrating Time-Dependent Histopathology.

Chamninawakul Padol P, Lim Ziying Vanessa ZV, Khoo Lawrence Shih Wee LSW, Lee Joyce Siong See JSS

Fixed drug eruption (FDE) is classically a lymphocyte-predominant interface dermatitis, but an early lesion may show a prominent neutrophilic infiltrate that closely simulates a primary neutrophilic dermatosis. We report 2 cases. The first, a 42-year-old woman, developed a multifocal eruption approximately 45 minutes after re-exposure to etoricoxib, recurring at previously affected and new sites. A punch biopsy performed 21 hours after ingestion of the drug showed a basketweave stratum corneum, intense papillary dermal edema with pseudovesiculation, and a superficial and deep infiltrate rich in neutrophils with karyorrhexis, closely resembling Sweet syndrome. Only occasional apoptotic keratinocytes were present within the epidermis, and the marked edema obscured any interface dermatitis, although admixed eosinophils were noted. Clinicopathologic correlation ultimately established the diagnosis of neutrophilic FDE. The second, a 55-year-old man, had an eruption recurring at the same sites after pseudoephedrine. A biopsy of an established lesion 2-3 weeks after ingestion showed classic interface dermatitis with numerous eosinophils and pigment incontinence, whereas one taken from the same region within 24 hours of re-exposure showed a neutrophil-predominant infiltrate with prominent karyorrhexis and only focal interface change. These cases, biopsied at documented time points, support the concept that the neutrophil-rich appearance of FDE represents an early phase in its histopathologic evolution, demonstrate how it can be mistaken for a neutrophilic dermatosis in the absence of adequate clinical history, and show that clinicopathologic correlation and a high index of suspicion are necessary to reliably arrive at the correct diagnosis.

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PubMedOncoimmunology2026-10-13

Estradiol-associated extracellular signaling in the human breast in vivo identifies mast cells as tumor-supportive stromal mediators.

Abrahamsson Annelie A, Wang Xingyue X, Zhong Wen W, Dabrosin Charlotta C

Sex steroid exposure is a major risk factor for breast cancer initiation and progression through incompletely understood mechanisms. Novel therapeutics for prevention and treatment of estrogen-dependent breast cancer are needed. Cell-cell interactions within the microenvironment contribute to breast cancer progression through extracellular signaling. Here, extracellular proteins were sampled directly from live normal human breast tissue and breast cancers using microdialysis, and 1,101 proteins were quantified. Mechanistic studies were performed in cultured intact normal human breast tissue and mast cells. Findings were validated in vivo using ER+ breast cancer models in immunocompetent and immunocompromised mice and in a zebrafish xenograft model. We identified a breast tissue-specific extracellular protein signature comprising 150 proteins associated with local estradiol (E2) levels, of which several were linked to mast cell biology, including stem cell factor (SCF). Human ER+ breast tumors exhibited increased extracellular SCF levels and higher mast cell density, which was associated with poorer overall survival. In normal human breast tissue, E2 increased mast cell abundance and activity. In vitro, E2 rapidly activated mast cells, an effect blocked by desloratadine. In mouse breast cancer models, E2 increased and fulvestrant reduced mast cell density. In the zebrafish, mast cells promoted ER+ breast cancer growth, which was further enhanced by E2 and abrogated by desloratadine. Overall, our findings identify mast cells as estrogen-responsive stromal mediators and support targeting mast cell-dependent pathways as a potential strategy for the prevention and treatment of estrogen-dependent breast cancer.

PMID 42868199
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PubMedAdvanced biotechnology2026-10-11

Spatial multi-omics uncovers an invasive-desmoplastic cellular community with prognostic and therapeutic implications in pancreatic ductal adenocarcinoma.

Liang Chang-Hao CH, Ye Hua H, Xu Hui H, Fang Chen C et al.

Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense desmoplastic stroma and profound spatial heterogeneity, yet the multicellular organizational principles governing its tumor microenvironment remain poorly understood. Here, we performed single-cell RNA sequencing (scRNA-seq; n = 9) and spatial transcriptomics (n = 4), integrating 61,234 single cells and 30,430 spots to identify an invasive-frontier myofibroblastic cancer-associated fibroblast (IF-myCAF), which is characterized by elevated expression of ACTA2, TAGLN, COL11A1, THBS2, CTHRC1, and POSTN. IF-myCAFs were validated in eight independent PDAC cohorts (159 samples with 67,959 CAFs), showing conserved transcriptional programs and representing a major CAF subpopulation across datasets. Spatial cellular community (CC) analysis identified five recurrent CCs that delineated the multicellular organization of PDAC. Notably, the invasive-desmoplastic CC (ID-CC), which localized to the tumor-stroma interface, was defined by a 5.8-fold enrichment of IF-myCAF; within this community, IF-myCAF colocalized with malignant ductal cells and macrophages. We also found that the ID-CC transcriptional signature was independently associated with worse outcome in TCGA-PAAD. Furthermore, ligand-receptor (LR) analysis of 4,009 IF-myCAF-associated LR pairs identified IF-myCAF as the predominant cell population mediating ECM-related intercellular signaling within ID-CC. Structure-based virtual screening against four IF-myCAF-derived ligand-receptor axes mediating intercellular communication within this community (THBS2-CD47, CTHRC1-FZD8, PPIA-BSG/CD147, MIF-CD74) identified five multi-target drug-repurposing candidates, including conivaptan, lonafarnib, rucaparib, desloratadine, and ketotifen. Collectively, this study first identified a novel CAF subpopulation, IF-myCAF, and established a CC-based organizational scheme for PDAC spatial architecture. Our findings advance our understanding of spatial ecosystem-level stromal heterogeneity in PDAC and suggest targeting IF-myCAF-driven signaling within ID-CC.

PMID 42859340
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