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sildenafil citrate (HCP 1207 / Pahtension / HGP 1207)

✓ Approved

Hanmi Pharmaceutical · PDE5A · 小分子

什么是 sildenafil citrate？

sildenafil citrate 是一种小分子，由Hanmi Pharmaceutical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HCP 1207, Pahtension, HGP 1207
公司Hanmi Pharmaceutical
药物类别小分子
分子靶点PDE5A
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Hanmi Pharmaceutical

作用机制

分子靶点

sildenafil citrate 作用于 1 个分子靶点：

PDE5Aphosphodiesterase 5A (PDE5, CGB-PDE)
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

sildenafil citrate 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
Respiratory, thoracic and mediastinal disordersPulmonary hypertension✓ Approved

相关研究文献

PubMedJournal of perinatology : official journal of the California Perinatal Association2026-09-11

Magnesium therapy in persistent pulmonary hypertension of the newborn: a scoping review.

Dadon Yuval Y, Mimouni Francis B FB, Arad Iris I, Mendlovic Joseph J

To map evidence on magnesium sulfate (MgSO₄) therapy for PPHN, focusing on efficacy, safety, mechanisms, and knowledge gaps. Scoping review following JBI methodology and PRISMA-ScR. MEDLINE, Embase, Cochrane Reviews, and CENTRAL were searched without date restrictions. Thirteen publications were included: 11 primary clinical reports, including three randomized trials, and two evidence syntheses. The primary reports included 253 neonates but differed in populations, severity, comparators, and outcomes. Intravenous MgSO₄ usually comprised a 200 mg/kg loading dose followed by continuous infusion. Small, mostly uncontrolled studies reported improved oxygenation but could not establish efficacy. Comparative studies showed slower or less consistent responses than inhaled nitric oxide or sildenafil. Adverse effects included hypotension, bradycardia, and increased inotropic requirements; long-term safety data were limited. Evidence remains insufficient to support routine MgSO₄ use for PPHN.

PMID 42722769
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PubMedBiotechnology journal2026-09-11

Metabolic Footprint of Drosophila S2 Cells: Findings During the Production of a Recombinant Rabies Virus Glycoprotein.

Decarli Monize Caiado MC, Dos Santos Diogo Peres DP, Correia Daniela Matilde DM, de Azevedo Amadeus Gomes AG et al.

Over the past 50 years, the Drosophila melanogaster S2 cells have been valued for their ability to synthesize therapeutic molecules at high yield. To further increase protein expression, it is imperative to improve cellular performance, which is intrinsically linked to cell metabolism. Nevertheless, information on S2 metabolism, including pathways, components, and cellular compartments, remains limited, hindering advances in S2 cellular performance. Herein, using a genetically modified S2 cell line expressing the recombinant rabies virus glycoprotein (RVGP), we investigated the stress caused by RVGP production on S2 cells. Batch cultures using wild- and rec-types were performed, and 27 compounds were quantified over 192 h. The extracellular metabolome affected the rec-S2 growth kinetics after RVGP expression was activated. Although RVGP was produced in high amounts, we identified a substrate limitation for rec-S2 cell growth (glutamine), changes in amino acid routes due to RVGP biosynthesis (leucine, serine, glycine, and valine), and metabolites that might be affecting rec-S2 cell growth (acetate, pyruvate, citrate, and malate). Organic acid analysis indicated that malate and acetate production are correlated with RVGP production. This work revealed metabolic correlations in S2 cells that may have direct implications for media optimization and yield maximization, thereby improving S2 performance for scale-up.

PMID 42723328
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PubMedInternational journal of cardiology. Heart & vasculature2026-09-11

Multi-omics profiling of circulating proteins and metabolites in persistent atrial fibrillation: VDAC1 identified as a candidate circulating protein.

Wang Jun J, Chen Xiaozhen X, Zhang Zilan Z, Gui Chun C

Atrial fibrillation (AF) is the most common heart rhythm disorder worldwide. Changes in metabolism and damage to mitochondria affect left atrial structure and electrical function. Few studies have applied multi-omics to plasma from AF patients. We enrolled 37 patients with persistent AF and 36 with supraventricular tachycardia (SVT). Blood samples were drawn from the coronary sinus in all patients. Ten subjects from each group were randomly selected for 4D-DIA proteomics and untargeted metabolomics. ELISA validation was done on 35 patients per group. Four GEO atrial tissue datasets and one single-nucleus RNA-seq dataset were used for external support. Differentially expressed proteins (DEPs) were defined by |fold change| ≥ 1.5 and Benjamini-Hochberg adjusted P < 0.05. Protein-protein interaction networks were built with STRING and Cytoscape. We quantified 3268 plasma proteins and identified 217 DEPs in AF. Network analysis showed voltage-dependent anion channel 1 (VDAC1) as a central mitochondrial hub. It connected respiratory chain subunits and autophagy regulators. ELISA confirmed higher plasma VDAC1, citrate synthase(CS) and secreted frizzled-related protein 2(SFRP2) in AF patients (all P < 0.001). Metabolomics identified 505 differentially abundant compounds. Glycerophospholipid and fatty acid pathways were disrupted. Integrated analysis revealed eight shared dysregulated pathways linked to energy metabolism. Four GEO datasets showed higher atrial VDAC1 transcripts in AF (P < 0.05). Single-nucleus RNA-seq localized VDAC1 to cardiomyocytes. Plasma protein and metabolite profiles differ between persistent AF and SVT. Mitochondrial and lipid pathways are both affected. VDAC1 is elevated in plasma, atrial tissue. These findings are supported across multiple cohorts.

PMID 42724651
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PubMedFrontiers in pharmacology2026-09-11

Integrated untargeted and targeted metabolomics combined with experimental validation reveal glutathione-related oxidative stress in pediatric IgA vasculitis nephritis.

Xi Leying L, Xu Xiaoqi X, Xing Qionqiong Q, Xu Shuang S et al.

IgA vasculitis nephritis (IgAVN) is the principal cause of morbidity and mortality in children with IgA vasculitis (IgAV),the pathogenesis of the renal injury and predictive biomarkers are still unclear. In this study, we performed an integrated untargeted and targeted metabolomics to identify candidate biomarkers and explore oxidative stress-related alterations associated with IgAVN. Serum samples were collected from 115 IgAV and 111 IgAVN children. We conducted untargeted metabolomics for preliminary screening of potential biomarkers on 50 IgAV and 50 IgAVN children and then performed validation experiments based on targeted LC-MS/MS on 65 IgAV and 61 IgAVN children. In addition, an IgAVN animal model was established to preliminarily verify oxidative stress-related alterations associated with key metabolic abnormalities by assessing the levels of GSH, GSH/GSSG, MDA, 4-HNE, NRF2, HO-1, and GPX4. A total of 45 differential metabolites were identified between the IgAV and IgAVN groups, including 23 upregulated and 22 downregulated metabolites, which were mainly enriched in glutathione metabolism, pyruvate metabolism, the citrate cycle, sphingolipid metabolism, and steroid hormone biosynthesis. Further targeted validation confirmed that six metabolites, including sphinganine, dehydroepiandrosterone, kynurenine, glutathione, nervonic acid, and creatine differed significantly between the two groups. The combined model based on these six metabolites showed good discriminatory performance, with an AUC of 0.903 and an area under the PRC curve of 0.909. In the animal experiments, the model group exhibited decreased GSH levels, a disrupted GSH/GSSG balance, increased MDA and 4-HNE levels, as well as abnormal expression of NRF2, HO-1, and GPX4. Children with IgAVN exhibit a distinct metabolic profile characterized by glutathione depletion, activation of inflammation-related tryptophan metabolism, lipid/membrane remodeling, and disordered energy metabolism. Sphinganine, dehydroepiandrosterone, kynurenine, glutathione, nervonic acid, and creatine may serve as potential biomarkers for IgAVN, and the combined model based on these metabolites showed good discriminatory ability and potential clinical utility. The consistency between the clinical metabolomics findings and the experimental evidence supports supports glutathione-related oxidative stress and the GSH-NRF2/HO-1/GPX4 axis as candidate pathways associated with IgAVN-related renal injury. These findings provide a basis for early risk identification and future mechanistic and pharmacological investigations in pediatric IgAVN.

PMID 42723862
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PubMedThe Journal of physiology2026-09-11

Preserved mitochondrial respiration in presence of oxidative stress and reduced mitochondrial mass after 10-day bed rest in older adults.

Motanova Evgeniia E, Zuccarelli Lucrezia L, Lysenko Evgenii E, Amoretti Stefano S et al.

Ageing affects mitochondrial integrity in skeletal muscle, and physical inactivity may further exacerbate these changes. Although mitochondrial alterations are documented in ageing and disuse independently, how disuse impacts the mitochondrial phenotype in older populations remains unclear. This work aimed to characterise how physical inactivity impacts mitochondrial function, morphology and gene expression in the skeletal muscle of older adults. Ten healthy older men (65+ years) underwent 10 days of bed rest. Skeletal muscle biopsies were collected before and after bed rest to assess mitochondrial respiration (high-resolution respirometry), H2O2 emission, mitochondrial protein expression, morphology and volume density (electron microscopy) and transcriptomic profile. Ten days of inactivity increased mitochondrial reactive oxygen species (ROS) emission under non-phosphorylating conditions but did not impair oxidative phosphorylation (OXPHOS) capacity, indicating preserved respiratory efficiency. Consistently, mitochondrial respiratory complex and supercomplex protein abundance were unchanged. Mitochondrial mass decreased, as shown by reduced mitochondrial volume density. Reduced dynamin-like protein 1 (DRP1) phosphorylation at serine 637 was observed, whereas other mitochondrial fission and fusion protein levels remained unchanged. Mitochondrial morphology remained unaltered. Transcriptomic analysis revealed >3000 differentially expressed genes, characterised by downregulation of oxidative phosphorylation genes alongside altered mitophagy, antioxidant and oxidoreductase pathways. In summary, 10-day bed rest increased mitochondrial ROS emission and reduced mitochondrial mass in older skeletal muscle despite preserved respiratory function, indicating that elevated ROS production occurs upstream of respiratory dysfunction and is potentially linked to impaired antioxidant defence and ROS clearance. These findings suggest that preserving redox balance during inactivity may be a key strategy to maintain muscle health and functional independence in ageing populations. KEY POINTS: The impact of short-term physical inactivity on mitochondrial function within the context of ageing remains poorly defined. This study examined the impact of 10-day bed rest on skeletal muscle mitochondrial function, morphology and gene expression in older adults. Short-term inactivity increased mitochondrial ROS production, accompanied by a dysregulation of antioxidant and oxidoreductase genes, indicating a reduced capacity for ROS clearance. Mitochondrial respiration was preserved under both submaximal and maximal stimulation. When normalised to mitochondrial content (citrate synthase activity), respiratory capacity increased, suggesting improved intrinsic efficiency. Mitochondrial mass was reduced, supported by decreased mitochondrial volume density assessed morphologically. Transcriptomic alterations in the mitophagy pathway suggest a potential role of altered mitochondrial degradation in this reduction. These findings indicate a transient compensatory response of ageing mitochondria to short-term disuse, suggesting that functional impairments are likely driven by cardiovascular and microvascular factors rather than mitochondrial respiration itself.

PMID 42723548
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PubMedFrontiers in oncology2026-09-10

A two-phase low-dose ACD-A strategy overcomes hypocalcemia during peripheral blood stem cell collection: a randomized controlled study.

Long Zhangbiao Z, Jin Yutong Y, Zhao Dinghui D, Li Yuxin Y et al.

Citrate anticoagulation during peripheral blood stem cell (PBSC) collection frequently causes hypocalcemia. Conventional fixed-ratio protocols frequently employ prophylactic calcium supplementation in many centers; however, they are associated with a high citrate burden and have been linked to platelet aggregation in some reports. This randomized controlled study evaluated a two-phase low-dose Acid Citrate Dextrose formula A (ACD-A) strategy designed to reduce hypocalcemia without compromising collection efficiency. Consecutive donors undergoing PBSC collection were randomly assigned to two groups. The Control group (n=22) received a blood-to-ACD-A ratio of 10-12:1 with prophylactic intravenous calcium. The Low ACD-A group (n=21) received initial loading phase at a ratio of 10-12:1 until 1 mL/kg of ACD-A was infused, followed by maintenance at 25:1 without prophylactic calcium. The primary outcome was the incidence of hypocalcemia-related symptoms. Secondary outcomes included collection time, ACD-A intake, CD34+ cell yield, and platelet aggregation. The incidence of hypocalcemia-related symptoms was significantly lower in the Low ACD-A group than in the Control group (14% vs. 73%, P = 0.0002). Collection time was shorter (170.8 vs. 199.3 min, P = 0.0029), and ACD-A intake was substantially reduced (6.10 vs. 12.96 mL/kg, P < 0.0001). No significant differences were observed in CD34+ cell yield, enrichment ratio, yield per liter processed, or changes in ionized calcium levels between groups. Mild platelet aggregation occurred less frequently in the Low ACD-A group (9.5% vs. 41%, P = 0.0339). A two-phase low-dose ACD-A strategy significantly reduces hypocalcemia-related symptoms, shortens collection time, and decreases platelet aggregation without compromising stem cell yield or product quality. This simple modification represents a meaningful improvement over conventional citrate protocols for PBSC collection.

PMID 42718461
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