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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)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

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

PubMedJournal of clinical apheresis2026-10-15

Apheresis in Children of Weight Under 7 kg-A Single Center Experience.

Rungsiprakarn Phassawan P, Wilson Bryan E BE, Rintoul Natalie E NE, Wild K Taylor KT et al.

Although apheresis techniques in children are well established, published experience with very low-weight children is limited. We reviewed 68 procedures performed in 19 children weighing less than 7 kg, including hematopoietic progenitor and T-cell collections and plasmapheresis. With significant modifications of standard techniques, all but one procedure was successfully and safely completed without serious citrate toxicity. Access was a major challenge. For plasmapheresis, the mean plasma volume removed was 1.2 × total plasma volume, but the mean total blood processed was 1.74 × total blood volume (TBV). For collections, the mean number of whole blood volumes processed was 4.1 × TBV. For T cell collections, the median CD3+ yield was 243.6 × 106/kg. For HPC collections, the median CD34+ cell yield was 14.8 × 106/kg. Mean durations for collections and plasmapheresis were 247.00 and 120.67 min, respectively. Of the CBC parameters, only platelet count was significantly lower after collections.

PMID 42875967
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PubMedPharmacological reports : PR2026-10-15

GLS2 reshapes glycolytic metabolism and bioenergetic homeostasis in glioblastoma cells.

De Los Santos-Jiménez Juan J, Campos-Sandoval José A JA, Sudderth Jessica J, Zacharias Lauren G LG et al.

Glioblastoma (GBM) exhibits extensive metabolic reprogramming, including glucose and glutamine (Gln) addiction, with Gln being converted into glutamate by glutaminase, encoded by the GLS and GLS2 genes. GLS2 acts as a context-dependent tumor suppressor, although the underlying mechanisms remain poorly understood. GLS2 is silenced in GBM, and we previously showed that its re-expression modulates pyruvate dehydrogenase (PDH) activity and tricarboxylic acid cycle (TCAC) metabolism, suggesting a distinct metabolic rewiring associated with its tumor-suppressive function. LN229 and T98G GBM cell lines were used as experimental models. Metabolomic profiling by liquid chromatography-mass spectrometry was performed to compare changes in central metabolic pathways following GLS2 or GLS overexpression. Glutaminase and PDH enzymatic activities were measured, and Western blotting was performed to assess GLS, GLS2, and PDHA1 protein levels and PDHA1 phosphorylation. A Seahorse analyzer was employed to quantify real-time ATP production derived from glycolysis and oxidative phosphorylation. Overexpression of GLS2, but not GLS, in LN229 cells caused the accumulation of TCAC-related metabolites, except for citrate, whose depletion is attributed to GLS2's effect on PDH phosphorylation, causing reduced PDH activity. This was accompanied by decreased levels of several acyl-carnitines. Furthermore, GLS2 induced the accumulation of glucose/fructose, while reducing levels of glucose-6-phosphate and pentose-phosphates, consistent with altered glycolysis. GLS2 also diminished the ATP/AMP ratio, confirmed by a reduced ATP synthesis rate, particularly glycolytic ATP, whereas mitochondrial ATP production remained unaltered. GLS2 exerts an isoenzyme-specific effect on Gln and glucose metabolism in GBM, likely modulating the glycolysis/pentose-phosphate pathway (PPP)-TCAC-axis.

PMID 42875721
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PubMedDrugs2026-10-15

Metformin Lowers Fasting Hyperglycemia by Increasing Glucose Clearance in People with Moderately Controlled Type 2 Diabetes.

Kahl Sabine S, LaMoia Traci E TE, Jonuscheit Marc M, Heilmann Geronimo G et al.

Metformin is the most frequently prescribed antidiabetic drug worldwide; however, the mechanism by which it lowers blood glucose remains incompletely understood. The objective of this study was to examine the effects of metformin on whole-body and specifically on hepatic glucose and energy metabolism in type 2 diabetes. This open repeated-measures pilot study examined this question using Positional Isotopomer NMR Tracer Analysis (PINTA) to assess rates of endogenous glucose production (VEGP), hepatic pyruvate carboxylase flux (VPC), and citrate synthase (VCS) flux in 16 men with moderately controlled type 2 diabetes (T2D; BMI 30 ± 3 kg/m2, HbA1c 8.4 ± 1.4%) undergoing two examination days with (M+; 1 g twice daily) and without metformin (M-) treatment. Hepatic ATP and glycogen concentrations were quantified by 31P/13C magnetic resonance spectroscopy. M+ reduced fasting glycemia by 18%, which could mostly be attributed to a 24% increase in rates of whole-body glucose clearance. Surprisingly, these changes were accompanied by a 58% increase in VPC and a 34% increase in VCS, due to a 26% increase in plasma glucagon concentrations. The increase in VPC was offset by reductions in the contributions of glycerol conversion to glucose resulting in no change in VEGP. Metformin decreased hepatic ATP content by 16% and increased plasma GDF-15 concentrations, but did not alter rates of net hepatic glycogenolysis. Metformin treatment in male individuals of European ancestry with moderately controlled T2D decreases blood glucose concentrations by increasing rates of whole-body glucose clearance. Metformin further inhibits glycerol-derived gluconeogenesis, which is consistent with complex IV, not complex I, being the molecular target of metformin action. ClinicalTrials.gov ( https://clinicaltrials.gov/ ): NCT04088851.

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PubMedPlastic and reconstructive surgery2026-10-14

Optimizing Concentrated Growth Factor Therapy: Sodium Citrate Reduces Pain in Hair Loss Treatment.

Pan Wenxing W, Chen Xinyi X, Li Haoyang H, Miao Zechen Z et al.

Androgenetic alopecia (AGA) is a prevalent condition causing significant psychosocial distress. While concentrated growth factor (CGF) therapy has emerged as a promising regenerative treatment, the choice of anticoagulant remains a critical but underexplored variable that may affect the growth factor release, and patient experience. To compare the efficacy, procedural pain, and patient satisfaction of CGF prepared with sodium citrate, heparin sodium, or no anticoagulant in patients with AGA. This phase 2, multicenter, single-blind, randomized controlled trial enrolled 267 patients aged 18 to 50 years across three tertiary hospitals in China. Participants were randomized 1:1:1 to receive CGF prepared without anticoagulant (Group A), with 3.2% sodium citrate (Group B), or with heparin sodium (Group C). All patients underwent five intradermal injection sessions over 12 months. Primary endpoints included injection-related pain (VAS) and changes in hair density at 3, 6, and 12 months. Injection pain was significantly lower in Group B (P < 0.001). At 6 and 12 months, Group B demonstrated significantly greater hair density increases and higher rates of ≥50% subjective clinical improvement (P < 0.001). In vitro analysis confirmed that sodium citrate best preserved growth factor levels and platelet function. Overall satisfaction and willingness for re-treatment were highest in Group B (87.6%). Sodium citrate provided the most favorable balance of procedural tolerability, delivery reliability, and clinical efficacy. These findings support sodium citrate as the preferred anticoagulant for CGF preparation in AGA, while confirmation in broader populations and phase 3 trials is warranted.

PMID 42873090
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PubMedJournal of enzyme inhibition and medicinal chemistry2026-10-14

Research progress on ATP-citrate lyase and its inhibitors: a metabolic-epigenetic perspective.

Liu Qinglin Q, Sun Hongbin H, Dai Liang L

ATP-citrate lyase (ACLY) is a key enzyme in cellular metabolism that catalyses the cleavage of citrate to produce acetyl coenzyme A (acetyl-CoA), thereby bridging energy metabolism and epigenetic regulation. Acetyl-CoA serves as a common substrate for de novo lipogenesis (DNL) and histone acetylation. Aberrant ACLY activity is closely associated with various pathological conditions, including metabolic diseases, Immune-mediated inflammatory diseases (IMIDs), cancer, and neurodegenerative diseases, positioning ACLY as an important therapeutic target for these diseases. However, existing inhibitors face challenges such as insufficient selectivity and limited clinical efficacy and off-target effects. This review systematically summarises the molecular mechanisms and pathological significance of ACLY within the overarching framework of its dual metabolic-epigenetic functions, from three perspectives, namely its structure and function, disease relevance, and inhibitor development and optimisation strategies, aiming to provide a theoretical foundation for precision therapies targeting ACLY.

PMID 42875375
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PubMedBiochimica et biophysica acta. Molecular basis of disease2026-10-14

Purine and citrate metabolism in urolithiasis and bladder cancer: An integrated genetic, gene-expression, and targeted metabolite analysis.

Wigner-Jeziorska Paulina P, Grębowski Radosław R, Tokarz Paweł P, Plażuk Damian D et al.

Metabolic reprogramming is a hallmark of bladder cancer (BC), but the contribution of inherited variation in purine and citrate metabolism remains incompletely understood. Because urolithiasis shares selected metabolic and epidemiological features with BC, we compared both disorders to identify shared and disease-specific molecular patterns. We analysed polymorphisms in ACLY, XDH, PNP, HPRT1, and GART together with targeted gene expression in peripheral blood-derived RNA and urinary citrate, hypoxanthine, and glycine measured by 1H NMR in a Polish case-control cohort. Genetic associations were assessed using multivariable models adjusted for age, sex, smoking, and BMI, with BH-FDR correction. Genotype-expression, genotype-metabolite, and expression-metabolite relationships were evaluated, and peripheral findings were compared with GSE13507 and TCGA-BLCA bladder-tissue data. ACLY rs2304497 was associated with both diseases, whereas PNP rs1713420 showed a BC-specific association after multivariable adjustment and BH-FDR correction. XDH rs2295475 associations did not remain significant after multiple-testing correction, and formal interaction analyses provided no BH-FDR-significant evidence of effect modification. Peripheral ACLY and GART transcript abundance was lower in both disease groups, while PNP was additionally lower in urolithiasis. Urinary citrate and hypoxanthine were reduced only in urolithiasis. No cross-layer associations remained significant after adjustment and BH-FDR correction. In external bladder tissue, GART was increased in both datasets, while ACLY and HPRT1 were increased in paired TCGA-BLCA tumours. The findings indicate shared and disease-specific molecular patterns but do not support a simple linear relationship between inherited variation, peripheral transcript abundance, and urinary metabolites. Direct functional and tissue-specific validation is required.

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