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sildenafil citrate (HCP 1207 / Pahtension / HGP 1207)

✓ Approved

Hanmi Pharmaceutical · PDE5A · Small Molecule

What is sildenafil citrate?

sildenafil citrate is a small molecule developed by Hanmi Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesHCP 1207, Pahtension, HGP 1207
CompanyHanmi Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetPDE5A
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Hanmi Pharmaceutical

Mechanism of Action

Molecular Targets

sildenafil citrate acts on 1 molecular target:

PDE5Aphosphodiesterase 5A (PDE5, CGB-PDE)
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Therapeutic Indications

sildenafil citrate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Respiratory, thoracic and mediastinal disordersPulmonary hypertension✓ Approved

Related Research Articles

PubMedLaboratory medicine2026-09-20

Effect of sodium citrate and magnesium sulphate anticoagulation on platelet parameters measured on the Alinity hq analyzer.

Betzer Cristine C, McGrail Rie R

EDTA-dependent pseudothrombocytopenia (PTP) may cause spuriously low platelet counts and can be prevented by using alternative anticoagulants, such as sodium citrate (citrate) and magnesium sulphate (MgSO4). However, these anticoagulants may affect platelet parameters depending on the analytical platform. Their effect on platelet measurements using the Abbott Alinity hq hematology analyzer has not previously been evaluated. Blood samples from 40 outpatients without known PTP were collected in K2-EDTA, citrate, and MgSO4 tubes. Platelet count, mean platelet volume, and reticulated platelet fraction were measured on an Alinity hq analyzer. Paired comparisons were performed using Friedman repeated-measures analysis with the Dunn multiple comparisons test. Compared with EDTA, median platelet counts were statistically significantly lower in citrate (-21.1%) and MgSO4 (-31.7%) than in EDTA (P < .05). Mean platelet volume was also statistically significantly reduced in citrate (-3.2%) and MgSO4 (-4.7%) (P < .05). Median reticulated platelet fraction was slightly higher in both anticoagulants, but only MgSO4 differed substantially from EDTA. On the Alinity hq analyzer, citrate and MgSO4 result in statistically significantly lower platelet count than EDTA in samples from individuals without known PTP. Platelet parameters are therefore influenced by anticoagulant choice and should not be interpreted interchangeably.

PMID 42763434
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PubMedLipids in health and disease2026-09-20

Real-world use of bempedoic acid for hypercholesterolaemia: a German multicentre, retrospective, cohort study.

Haberbosch Linus L, Baessler Andrea A, de Ruiter Ulrike U, Sinning David D et al.

Dyslipidaemia remains a leading cause of death in Germany despite an improving therapeutic landscape, with many patients not achieving guideline-recommended low-density lipoprotein cholesterol (LDL-C) goals. Bempedoic acid, an adenosine triphosphate citrate lyase inhibitor, is a recent addition to the therapeutic landscape with proven efficacy in randomised controlled trials; however, its use varies between centres. We aimed to assess the short-term, real-world effectiveness of bempedoic acid in lowering LDL-C levels in patients in Germany. This retrospective, observational study was conducted using data from patients with primary hypercholesterolaemia or mixed dyslipidaemia, collected before and approximately 3 months after initiating bempedoic acid in 7 specialised lipid outpatient clinics in Germany. Data were analysed from a total of 641 patients, with a mean age (standard deviation [SD]) of 63.2 (11.3) years. The addition of bempedoic acid significantly reduced LDL-C levels from a mean of 133.6 mg/dL at baseline to 101.8 mg/dL after 3 months (p < 0.001). The mean within-patient LDL-C reduction was 31.8 mg/dL and the mean patient-level percentage change was -17.5%. Mean patient-level changes were -4.9% for HDL-C and -12.0% for total cholesterol; triglycerides did not change significantly. At 3 months, patients not receiving any lipid-lowering therapy (LLT) other than bempedoic acid had a mean patient-level LDL-C reduction of 27.1%; corresponding mean reductions were 23.7% with ezetimibe, 20.3% with PCSK9 inhibitor therapy, 9.0% with statin therapy and 6.1% with statin plus ezetimibe. Suspected adverse events were documented in 218/641 patients (34.0%), and 171/641 (26.7%) had discontinued bempedoic acid by follow-up. Myalgia was the most commonly reported adverse event in patients discontinuing treatment (75 cases). Findings from this real-world, multicentre study conducted in Germany show that bempedoic acid may present an effective treatment option for patients with hypercholesterolaemia who are already receiving LLT, in addition to being an effective option for patients not receiving/tolerating other LLTs. The magnitude of LDL-C reduction differed across background treatment strategies, while suspected adverse events and treatment discontinuation were common in this specialist-care cohort.

PMID 42763399
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PubMedBritish journal of clinical pharmacology2026-09-19

CYP3A5 genetic variability influences sildenafil and metabolite in pulmonary hypertension.

Wongwien Pranisa P, Pussadhamma Burabha B, Kanjanawart Sirimas S, Areesinpitak Thikhumporn T et al.

Interindividual variability in sildenafil response among pulmonary hypertension patients (PH) may be influenced by CYP3A5 polymorphisms. CYP3A5*3 allele reduces CYP3A5 activity and affects sildenafil metabolism. This study investigated the associations between CYP3A5 genotype and plasma concentrations of sildenafil and N-desmethyl sildenafil, as well as clinical outcomes, in PH. A cross-sectional study of 92 patients with PH was conducted. Blood samples were collected at trough and 1 h after sildenafil administration (C1h). Plasma concentrations were quantified by HPLC, and CYP3A5 genotypes were determined by real-time PCR with TaqMan probes. Thirteen (14.13%) patients carried the CYP3A5 *1/*1 genotype, and 79 (85.87%) carried the CYP3A5*3 allele. CYP3A5*3 allele carriers had a significantly higher mean C1h sildenafil concentration-to-dose (C/D) ratio than CYP3A5*1/*1 carriers (3.61 ± 2.69 vs. 2.66 ± 1.20 ng/mL/mg; p = 0.043). The mean C1h of sildenafil, trough sildenafil concentration and trough sildenafil C/D ratio were higher in CYP3A5*3 carriers, but not statistically significant. The trough and C1h of N-desmethyl sildenafil and their corresponding C/D ratios were lower in CYP3A5*3 carriers but did not reach statistical significance. CYP3A5*3 allele carriers showed greater improvement in 6-min walk distance (33.74 ± 43.46 m vs. -5.58 ± 44.52 m; p = 0.005), WHO functional class (32.00% vs. 15.39%; p = 0.042) and EmPHasis-10 scores (-4.15 ± 6.46 vs. 1.08 ± 3.80; p = 0.009). The CYP3A5*3 allele is associated with higher sildenafil exposure and superior clinical outcomes. Therefore, CYP3A5 genotyping may facilitate personalized assessment of sildenafil efficacy and clinical outcomes.

PMID 42760608
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PubMediScience2026-09-19

The mechanism of vascular injury caused by polystyrene microplastics: Involving ferroptosis and metabolomics.

Zhu Deyu D, Liang Xiao X, Huang Qi Q, Wu Yang Y et al.

Polystyrene microplastics (PS-MPs) are environmental pollutants linked to cardiovascular diseases. This study investigated PS-MP-induced vascular toxicity mechanisms in mice. Mice were divided into saline control, low/medium/high PS-MP exposure (0.1, 1, and 10 mg/kg/d), and PS-MPs plus ferroptosis inhibitor Ferrostatin-1 (1 mg/kg/d + Fer-1) for 5 weeks. Vascular histopathology, lipid profiles, oxidative stress, ferroptosis markers, endothelial function, and serum metabolomics were assessed. PS-MP exposure elevated ROS, MDA, TC, and TG while reducing GSH and HDL-C. Ferroptosis was confirmed by decreased GPX4 and SLC7A11, with increased Fe2+ deposition. Vascular endothelial injury and remodeling occurred, evidenced by elevated ET-1, VEGF-A, VCAM-1, and ICAM-1, alongside reduced NO. Metabolomics revealed disruptions in folate, amino acid, citrate cycle, and tryptophan metabolism. Fer-1 inhibited ferroptosis, alleviating endothelial damage and vascular remodeling. PS-MPs induce vascular toxicity through oxidative stress, ferroptosis, and metabolic disturbances, mitigated by Fer-1.

PMID 42761273
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PubMedFrontiers in pharmacology2026-09-19

Liraglutide and renal mitochondrial homeostasis: targeting the "metabolism-inflammation-lithogenesis" axis in metabolic syndrome.

Wang Fei F, Li Qiuyu Q, Wen Quan Q, Su Boyan B et al.

Nephrolithiasis associated with metabolic syndrome represents a growing global public health burden with a 5-year recurrence rate of up to 50%. Current first-line preventive strategies, primarily potassium citrate and thiazide diuretics, only correct urinary chemical abnormalities symptomatically, and patient adherence remains below 50% at 1 year. Importantly, these approaches fail to address the core pathological basis of tubular injury driven by metabolic dysregulation. Mitochondrial dysfunction is the central mechanistic hub linking systemic metabolic stress to intrarenal lithogenic susceptibility. In the setting of metabolic syndrome, impaired mitochondrial biogenesis and excessive mitochondrial reactive oxygen species (mtROS) production in renal tubular epithelial cells activate the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, establishing a self-perpetuating vicious cycle of "metabolic disturbance, mitochondrial damage, inflammatory amplification, calcium oxalate crystal deposition'. This core pathogenic loop has not been targeted by existing therapeutic strategies. Liraglutide, a long-acting glucagon-like peptide-1 receptor agonist (GLP-1RA), exerts pleiotropic renoprotective effects independent of its canonical glucose-lowering actions. It coordinately activates peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) through two complementary pathways: transcriptional upregulation through the PKA/CREB axis, and post-translational deacetylation via the AMPK/SIRT1 pathway. This dual activation restores mitochondrial homeostasis, reprograms tubular lipid metabolism, attenuates oxidative stress, and suppresses inflammatory cascades. This review is the first to systematically integrate the mitochondrial pharmacology of liraglutide with the pathophysiology of nephrolithiasis. It critically appraises the strengths and limitations of preclinical and clinical evidence, identifies key knowledge gaps in the field, and proposes a phased translational research roadmap encompassing mechanistic validation, biomarker development, and clinical trial design. This work provides a solid theoretical foundation for repurposing GLP-1RAs for the prevention of this condition.

PMID 42761830
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PubMedCancer treatment and research communications2026-09-19

Metabolic Reprogramming Of Macrophages In Breast Cancer: Mechanisms And Therapeutic Implications.

Zhang Jiaoyu J, Yang Rui R

As key immune cells in the tumor microenvironment (TME), macrophages polarize into pro-inflammatory M1 or anti-inflammatory M2 phenotypes, with their functional states tightly linked to metabolic pathway dynamics. This review comprehensively examines macrophage metabolic reprogramming in glycolysis, lipid metabolism, glutamine metabolism, the pentose phosphate pathway (PPP), mitochondrial function, the tricarboxylic acid (TCA) cycle, and amino acid metabolism, while exploring their implications for breast cancer's immune microenvironment and therapeutic approaches. In M1 macrophages, glycolysis is significantly enhanced, promoting the inflammatory response through lactate accumulation and reactive oxygen species (ROS) production. Simultaneously, the TCA cycle is disrupted at the citrate and succinate nodes, leading to the accumulation of metabolic intermediates and further strengthening the pro-inflammatory phenotype. On the other hand, M2 macrophages depend on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO). They regulate epigenetic modifications through metabolites such as alpha-ketoglutarate (α-KG) to maintain anti-inflammatory and tissue repair functions. Breast cancer cells reprogram macrophages via glutamine competition and exosome secretion, driving M2 polarization to support tumor progression. Different molecular subtypes exhibit distinct metabolic features: triple-negative breast cancer (TNBC) shows high glycolytic activity and glutamine addiction, whereas hormone receptor-positive breast cancer relies more on exogenous amino acid uptake. Targeting glycolysis or glutamine metabolism can revert tumor-associated macrophages (TAMs) to an anti-tumor M1-like state, boosting immunity. Although metabolic intervention strategies (such as inhibiting key enzymes hexokinase 2 (HK2), glutaminase (GLS), or fatty Acid Binding Protein 4 (FABP4)) show therapeutic potential, existing studies still have limitations: the compensatory effects between metabolic pathways, tumor heterogeneity, and insufficient clinical translation. Emerging strategies, including metabolic checkpoint targeting, CAR-macrophages (CAR-M), and biomimetic nanocarrier-based delivery systems, hold promise for overcoming these challenges. In summary, in-depth elucidation of the molecular mechanisms underlying macrophage metabolic reprogramming and their metabolic crosstalk with breast cancer cells will provide new insights and novel therapeutic targets for the precise immunometabolic therapy of breast cancer.

PMID 42762607
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