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desloratadine + pseudoephedrine (Clarinex D / Aerinaze)

✓ Approved

Merck & Co. · HRH1 · Small Molecule

What is desloratadine + pseudoephedrine?

desloratadine + pseudoephedrine is a small molecule developed by Merck & Co.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesClarinex D, Aerinaze
CompanyMerck & Co.
Drug ClassSmall Molecule
Molecular TargetHRH1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Merck & Co.

Mechanism of Action

Molecular Targets

desloratadine + pseudoephedrine acts on 1 molecular target:

HRH1histamine receptor H1 (HH1R, H1R)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

desloratadine + pseudoephedrine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Immune system disordersSeasonal allergy✓ Approved

Related Research Articles

PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-05-22

NAT10-Mediated ac4C Modification of circANKRD12 Reprograms the Tumor Microenvironment.

Zhang Jiale J, Shi Hui H, Wang Chen C, Liu Zihao Z et al.

Developing anticancer strategies that simultaneously target both tumor proliferation and the immunosuppressive microenvironment remains a major challenge. However, the role of chemical modifications in circular RNAs (circRNAs) in this process remains poorly understood. In this study, we identified circANKRD12 as a key substrate for N4-acetylcytidine (ac4C) modification, catalyzed by N-acetyltransferase 10 (NAT10) in multiple myeloma (MM). This ac4C modification promotes the translation of circANKRD12 into a novel 354-amino acid protein (circANKRD12_354aa). Functionally, circANKRD12_354aa interacts with histone deacetylase 2 (HDAC2) to stabilize the oncoprotein c-Myc, thereby driving MM cell proliferation. Moreover, circANKRD12 could be transferred from MM cells to natural killer (NK) cells, where it similarly suppressed NK cell cytotoxicity via the HDAC2/c-Myc axis, facilitating immune evasion. Clinically, circANKRD12 was upregulated in MM patients and correlated with poorer prognosis. Through high-throughput screening, we further identified the clinical antihistamine desloratadine as a direct binder of circANKRD12_354aa. Targeting the circANKRD12/HDAC2/c-Myc axis with desloratadine effectively suppresses MM growth and restores NK cell-mediated antitumor immunity in vivo. Our study reveals that NAT10-mediated ac4C modification of circANKRD12 plays a central role in coordinating tumor proliferation and immune dysfunction, establishing circANKRD12_354aa as a promising therapeutic target for restoring antitumor immunity in MM.

PMID 42172090
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PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-05-11

Mahuang Fuzi Xixin decoction attenuates allergic rhinitis by suppressing MHC-II-mediated antigen presentation in ovalbumin induced murine model.

Wei Xiaohan X, Ding Mengze M, Tan Xiaomei X

Allergic rhinitis (AR) is a chronic condition that impairs daily life and imposes economic burdens. Mahuang Fuzi Xixin Decoction (MFXD) is a commonly employed herbal formula in China for treating AR, owing to its established clinical efficacy. However, investigations into its underlying mechanisms remain limited. To evaluate the therapeutic effects of MFXD in a mouse model of AR and to investigate its influence on antigen presentation, thereby elucidating potential mechanisms of action. An ovalbumin (OVA)-induced murine AR model was established to assess the efficacy of MFXD. Subsequently, data-independent acquisition (DIA) proteomics characterized differentially expressed proteins (DEPs) in the nasal mucosa following MFXD treatment, followed by pathway enrichment analysis. Guided by the proteomic findings, we examined the regulatory effects of MFXD on antigen presentation molecules in AR mice. Finally, human nasal epithelial cells (HNEpCs), dendritic cells (DC2.4), and Naïve CD4+ T cells isolated from OT-II mice were used to confirm the inhibitory effect of MFXD on the antigen presentation pathway. Additionally, chemical characterization of MFXD was performed. MFXD alleviated AR symptoms, mitigated histopathological alterations, and regulated plasma histamine and IgE levels, as well as IL-4, IL-13, and IFN-γ levels in the nasal lavage fluid (NLF) in AR mice. MFXD significantly reduced the number of nasal DEPs between AR and control groups, with the antigen processing and presentation pathway being the most prominently enriched. MFXD modulated splenic histopathology and spleen index, and decreased major histocompatibility complex class II (MHC-II) expression in both the nasal mucosa and spleen of AR mice. In vitro, MFXD diminished the antigen phagocytic capacity of lipopolysaccharide (LPS)-stimulated DC2.4 cells and lowered MHC-II and CD86 expression on both HNEpCs and DC2.4 cells; It also suppressed DC2.4-induced proliferation and differentiation of naive OT-II CD4+ T cells. MFXD also downregulated CD74, cathepsin S (CTSS), and MHC-II; this effect was partially reversed by the CD74 agonist MIF and by CD74 overexpression. This study explores one potential therapeutic mechanism of MFXD in AR. The findings suggests that MFXD may exert its therapeutic effect against AR by suppressing CD74/CTSS/MHC-II axis, thereby inhibiting antigen presentation. This work provides mechanistic insights that could inform the clinical use of MFXD and highlights potential targets for future AR drug development. Ephedrine, Pseudoephedrine, Methylephedrine, Benzoylmesaconine, Benzoylhypacoitine, Benzoylaconine, Asarone.

PMID 42107445
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PubMedOncogenesis2026-05-07

HPCAL1 promotes colorectal cancer progression via TCF7/p65-mediated Wnt ligand upregulation and Wnt/β-catenin pathway activation.

Cheng Linna L, Zhang Huiyang H, Guo Liqun L, Zhang Qing Q et al.

Abnormal Wnt/β-catenin pathway activation drives colorectal cancer (CRC) tumorigenesis, yet effective targeted therapies remain elusive. Given HPCAL1's established dual tumor-suppressive and oncogenic roles in other cancers, this study investigates its function in CRC to assess the therapeutic potential. Bioinformatic analyses of publicly available CRC datasets supported by in-house cohort studies linked high HPCAL1 expression in primary CRC tissues with clinicopathological factors associated with metastasis and worsened patient outcomes. Knockdown and overexpression studies in cell lines showed that HPCAL1 positively contributes to CRC cell motility and invasion, as well as proliferation in vitro and in vivo in xenografts. RNA sequencing linked HPCAL1 expression with the Wnt/β-catenin pathway, demonstrating positive correlations with Wnt ligands in CRC models and clinical samples. Biochemical approaches showed HPCAL1 augmented the activation and nuclear localization of β-catenin. Moreover, HPCAL1 formed distinct complexes with β-catenin in tandem with the TCF7 or p65 transcription factors, in turn, differentially transactivating Wnt6, Wnt7A, and Wnt11 ligands. Notably, the anticancer activity of desloratadine against CRC cells, a pharmacological inhibitor of HPCAL1, functioned by curtailing Wnt6, Wnt7A, and Wnt11 expression and suppressing Wnt/β-catenin signaling. Collectively, these findings indicate that HPCAL1 is a significant contributor to the clinical aggressiveness of CRC with oncogenic effects intrinsically linked with sustaining canonical Wnt pathway activation. Furthermore, drug targeting experiments provide proof-of-principle evidence for promoting HPCAL1 as a therapeutic target for countering activated Wnt/β-catenin signaling in colorectal cancer.

PMID 42091587
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PubMedCurrent research in pharmacology and drug discovery2026-05-01

Desloratadine attenuates renal ischemia-reperfusion injury through activation of the Nrf2-GCL-GSH antioxidant pathway.

Gholampour Firouzeh F, Maghsoodi Atefeh A, Malekmohammad Khojasteh K

Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) in transplantation and major surgery, with limited effective pharmacological interventions. This study evaluated the prophylactic effect of desloratadine, a second-generation H1-receptor antagonist with anti-inflammatory and antioxidant properties, on renal IRI. Twenty-one male Sprague-Dawley rats were randomly assigned to three groups (n = 7 each): Sham, I/R (45 min ischemia followed by 24 h reperfusion), and I/R + desloratadine (5 mg/kg, orally, 1 h prior to ischemia). After 24 h of reperfusion, renal function, oxidative stress markers, histopathology, and antioxidant gene expression were assessed. I/R significantly impaired renal function (increased plasma creatinine and urea, decreased creatinine clearance; P < 0.001), reduced effective free-water reabsorption, and increased oxidative stress (elevated TOS, reduced TAC and GSH; P < 0.01-0.001). Desloratadine significantly improved renal function, restored tubular concentrating ability, reduced oxidative stress, and increased GSH levels (P < 0.05-0.001 vs. I/R). At the molecular level, I/R upregulated Nrf2 and HO-1 expression but downregulated Gclc and Gclm, while desloratadine further enhanced Nrf2/HO-1 expression and restored Gclc/Gclm levels. Histological analysis confirmed attenuation of tubular injury. In conclusion, desloratadine pretreatment is associated with protection against renal IRI, potentially through modulation of the Nrf2-GCL-GSH antioxidant pathway and preservation of tubular function. These findings support its potential repurposing as an adjuvant strategy in settings at risk of renal ischemic injury.

PMID 42063900
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PubMedTissue & cell2026-05-01

Targeting oxidative stress, inflammation, and apoptosis: The protective role of desloratadine against vancomycin-induced testicular toxicity via the SIRT1/Nrf2/NF-κB axis.

Alshehre Sallwa M SM, Qusty Naeem F NF, Bokhari Bayan T BT, Rajab Bodour S BS et al.

Vancomycin (VCM), a glycopeptide antibiotic frequently employed against methicillin-resistant Staphylococcus aureus (MRSA), has been linked to testicular toxicity and impaired male fertility. This study explores the protective effects of desloratadine (DES), a non-sedating antihistamine, against VCM-induced testicular damage in rats. Adult male albino rats were allocated into four groups: control, DES-only, VCM-only, and combined VCM+DES. Hormonal assays, sperm analysis, histological scoring, and molecular evaluations were conducted to assess reproductive function, oxidative stress, inflammation, and apoptosis. VCM administration led to a significant decline in serum testosterone and a marked elevation in FSH and LH, indicating disruption of the pituitary-gonadal axis. Sperm motility decreased, while the number of abnormal and dead sperm forms increased. Histological analysis revealed degeneration of seminiferous tubules and reduced PCNA expression, reflecting impaired spermatogenesis. VCM additionally elevated malondialdehyde (MDA) levels and suppressed antioxidant enzymes, including SOD, CAT, GPx, and glutathione (GSH). This was accompanied by downregulation of Nrf2 and HO-1. Inflammatory markers (NF-κB, TNF-α, IL-6, IL-1β) were elevated. Apoptotic proteins, including P53, Bax, and caspase-3, were upregulated, while Bcl-2 was reduced. Notably, DES co-treatment reversed these effects, restoring hormonal balance, improving sperm quality, and enhancing testicular architecture. DES similarly was associated with upregulation of the AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1)/PGC-1α signaling pathway, which correlated with Nrf2/HO-1 activation and suppression of NF-κB-mediated inflammation and P53-driven apoptosis. DES exerts multifaceted protection against VCM-induced testicular damage by modulating oxidative stress, inflammation, and apoptosis, with SIRT1 pathway activation playing a central role, regulating mitochondrial biogenesis, enhances antioxidant defenses, and modulates inflammatory and apoptotic signaling. These findings highlight DES as a promising therapeutic agent for preserving male reproductive function during antibiotic therapy.

PMID 42061022
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PubMedBiomolecules & therapeutics2026-04-30

Pseudoephedrine Improves Chronic Obstructive Pulmonary Disease by Regulating Airway Senescence and Mitochondrial Function through PI3K/AKT/mTOR Axis.

Wu Lijuan L, Chen Fenqiao F, Zhang He H, Xu Wenzhong W et al.

Ephedra can improve chronic obstructive pulmonary disease (COPD). Pseudoephedrine (PSE) is a main active ingredients of ephedra. It has anti-inflammatory pharmacological properties. Its effect on COPD and its possible mechanism have not been elucidated. The COPD rat model was constructed by systemic cigarette smoke exposure combined with lipopolysaccharide (LPS) tracheal instillation. BEAS-2B cells were treated using cigarette smoke extract; PSE was administered for treatment. The senescence level of rat lung tissue and bronchial epithelial cells was evaluated through staining, immunofluorescence and western blot. The mitochondrial damage of rats and BEAS-2B cells was detected by transmission electron microscopy, JC-1 probe, MitoSOX Red probe and kits. In addition, the lung function indexes of rats were detected by animal lung function analysis system. Hematoxylin and eosin (HE) staining analyzed the pathological damage. Enzyme-linked immunosorbent assay (ELISA), kit and immunohistochemistry were used to evaluate inflammation and oxidative stress. Western blot detected phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) axis protein. PSE significantly reduced senescent cells, apoptosis rate and P21 level in rat lung tissue and BEAS-2B cells, significantly increased the levels of zonula occludens-1 (ZO-1)and adenosine triphosphate (ATP), restored mitochondrial structure, and visible mitochondrial cristae. It also inhibited reactive oxygen species (ROS) levels and mitochondrial excessive fission. PSE also significantly improved lung function in rats, increased mean alveolar number (MAN), reduced pro-inflammatory factors, and increased superoxide dismutase (SOD) levels. PSE markedly suppressed p-p85, p-AKT and p-mTOR protein expressions. In addition, the PI3K/AKT agonist 740Y-P weakened the effect of PSE on improving COPD. PSE inhibited PI3K/AKT/mTOR axis, improved lung tissue senescence, mitochondrial dysfunction and pathological damage, and reduced airway inflammation and oxidative stress damage, thereby alleviating COPD.

PMID 42059030
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