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sildenafil citrate (SPO1101D / Vultis / SPO1101)

✓ Approved

Seoul Pharmaceuticals · PDE5A · Small Molecule

What is sildenafil citrate?

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

Drug Profile

Brand NamesSPO1101D, Vultis, SPO1101
CompanySeoul Pharmaceuticals
Drug ClassSmall Molecule
Molecular TargetPDE5A
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Seoul Pharmaceuticals

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
Reproductive system and breast disordersErectile dysfunction✓ Approved

Related Research Articles

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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PubMedNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026-09-18

PDE5 inhibition restores mitochondrial function and improves neurobehavioral outcomes after repeated mild blast TBI.

Kilgore Madison O MO, Ye Shaojing S, Oyelami Felix F, Alareidi Alaa A et al.

Repeated mild traumatic brain injury (rmbTBI) is associated with persistent neurological deficits in military personnel arising from secondary cerebrovascular and metabolic impairments. Critically, there are no FDA-approved therapeutics for rmbTBI. Phosphodiesterase 5 (PDE5) inhibition has been explored in preclinical and clinical TBI studies; however, its exact therapeutic mechanism remains unclear. Recent data demonstrate that PDE5 inhibition can rescue mitochondrial dysfunction. As such, we hypothesized that PDE5 inhibition with sildenafil restores mitochondrial health following rmbTBI, conferring neurobehavioral improvement after rmbTBI. To model rmbTBI, male rats were exposed to two 11 psi blast waves 24 h apart, and daily sildenafil was initiated either 15 min or 8 weeks post-blast to assess subacute and delayed treatment effects. At 7 d post-injury, sildenafil restored rmbTBI-induced reductions in hippocampal expression of PGC-1α, a master regulator of mitochondrial biogenesis. Transcriptomic analysis revealed enrichment of oxidative phosphorylation pathways in sildenafil-treated animals, and metabolomic profiling indicated that rmbTBI results in cortical accumulation of glycolytic intermediates and altered NAD+ redox balance, both attenuated by sildenafil. To assess the mitochondrial signature of brain capillaries after PDE5 inhibition, we show that sildenafil restored mitochondrial bioenergetics in brain capillaries following AAPH-induced oxidative stress and rmbTBI. rmbTBI increased anxiety-like behavior at 3 d and 7 d post-injury, which was partially normalized by sildenafil. At 20 weeks, rmbTBI animals exhibited persistent fear-conditioned behavior, whereas sildenafil facilitated fear extinction. These findings demonstrate that rmbTBI disrupts mitochondrial function and behavior, and that PDE5 inhibition with sildenafil restores these alterations, supporting its potential as a therapeutic intervention for blast-induced TBI.

PMID 42759178
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PubMedCurrent opinion in critical care2026-09-18

Monitoring and dose adjustment of regional citrate anticoagulation for continuous renal replacement therapy.

Yessayan Lenar L, Szamosfalvi Balazs B, Tolwani Ashita A

Regional citrate anticoagulation (RCA) is the preferred anticoagulation strategy for many patients receiving continuous renal replacement therapy (CRRT). Safe implementation requires a coordinated prescription integrating citrate delivery, citrate removal within the extracorporeal circuit, individualized calcium replacement, CRRT fluid composition, and structured biochemical monitoring. This review summarizes practical approaches to RCA prescription, monitoring, and dose adjustment, emphasizing recent advances in citrate kinetics, calcium homeostasis, impaired citrate metabolism, metabolic complications, and systems-based safety. Randomized trials and meta-analyses continue to demonstrate that RCA prolongs circuit life and reduces bleeding compared with systemic heparin anticoagulation, although a mortality benefit has not been demonstrated. Recent studies have refined understanding of citrate dose, systemic citrate load, first-pass citrate extraction, individualized calcium replacement based on anticipated effluent calcium losses, and recognition of impaired citrate metabolism. They also support baseline ionized calcium assessment before CRRT initiation, integration of lactate trends into assessment of citrate metabolism, individualized CRRT fluid selection, and distinguishing true citrate accumulation from other metabolic effects of RCA. RCA is most effectively managed as an integrated CRRT prescription in which citrate delivery and removal, individualized calcium replacement, CRRT fluid composition, and operational parameters are coordinated to optimize circuit anticoagulation while maintaining electrolyte and acid-base homeostasis. Prescription adjustment should focus on four recurring clinical scenarios: inadequate circuit anticoagulation, negative calcium balance, excessive bicarbonate generation from citrate metabolism, and impaired citrate metabolism. Standardized protocols, structured monitoring, staff training, and workflow integration remain central to safe RCA implementation.

PMID 42758964
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PubMedInternational journal of biological macromolecules2026-09-18

Electrospun Zein/hydroxypropyl methylcellulose/silver citrate nanofibres with enhanced thermal and morphological stability for wound healing.

Aguila Marco Antonio Lopez MAL, Jia Jiaojiao J, Xu Yingde Y, Liang Yanqin Y et al.

Wound dressing is a critical in wound healing, yet natural electrospun nanofibres often lack thermal and morphological stability, limiting clinical utility. To address this, Zein nanofibrous mats with silver citrate nanorods (AgCit) were fabricated by electrospinning, crosslinked with citric acid (catalysed by sodium hypophosphite), and reinforced with hydroxypropyl methylcellulose (HPMC). FE-SEM revealed bead-free fibres at 5 mM AgCit, 40 wt% Zein, and 0.5 wt% HPMC, with an average diameter of 930 ± 5.5 nm. Morphological stability was achieved by HPMC reinforcement and AgCit, which prevent fibre collapse under aqueous immersion, while crosslinking was insufficient. Thermal stability was enhanced by citrate-Zein interactions and compact chain packing induced by HPMC, as confirmed by DSC (Tg1 above 100 °C) and TGA (reduced degradation rates). These strategies provided dual advantages: resilience under physiological conditions and improved durability during processing. Cell assays demonstrated cytocompatibility, proliferation, and migration, with AgCit supporting wound closure. Time-kill curves showed a 90.67 ± 0.49% and 92 ± 0.96% of antibacterial efficiency against E. coli and S. aureus, respectively within 9 h. The mechanism involves hydrogen bonding and chain entanglement between Zein and HPMC, reinforced by citrate crosslinking, while AgCit contributes antibacterial activity and HPMC provides antioxidant effect.

PMID 42759633
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PubMedMolecular biology reports2026-09-18

Mitochondrial metabolite transporters at the crossroads of metabolic reprogramming, epigenetic regulation and therapeutic vulnerabilities in colorectal cancer.

S Kaviya K, Arockiasamy Sumathy S, Srinivas K Satish KS, Shirley Sundersingh S

Metabolic reprogramming is a defining hallmark of CRC. The Warburg effect is the principal metabolic feature of CRC cells, wherein glucose is preferentially catabolized into lactate to sustain accelerated proliferation. In parallel, CRC cells exhibit strong glutamine reliance to replenish tricarboxylic acid (TCA) cycle intermediates required for adenosine triphosphate (ATP) production, lipid biosynthesis and redox homeostasis. Consequently, mitochondria play a central role in supporting the augmented biosynthetic and energetic demands beyond basal energy homeostasis. In this regard, the mitochondrial pyruvate carrier (MPC), mitochondrial citrate carrier (CIC) and the mitochondrial glutamine carrier (SLC1A5_var) located in the inner mitochondrial membrane, are emerging areas of investigation in CRC metabolism. MPC is frequently lost or downregulated in CRC, whereas CIC was found to be upregulated and promote CRC growth and survival. In contrast, SLC1A5_var has been reported to exhibit elevated expression in colon cancer cells. Recent evidence indicates that its inhibition reduces CRC cell viability; however, its specific role in CRC progression remains to be elucidated. Notably, these transporters may influence the metabolic-epigenetic landscape of CRC through metabolite-dependent regulation of chromatin and transcriptional processes. This review highlights current insights into mitochondrial metabolite transporters in CRC and their potential metabolic and epigenetic implications. Thus, elucidating the roles of these transporters may provide novel therapeutic strategies for CRC management.

PMID 42758364
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PubMedMolecular biomedicine2026-09-18

Induction of transferrin receptor 1-mediated ferroptosis by ultrasound-triggered microbubble destruction sensitizes glioblastoma to radiotherapy.

He Ying Y, Dong Xunhu X, Lu Xiaolu X, Zhu Qiong Q et al.

Ultrasound-triggered microbubble destruction (UTMD), a non-invasive technique, has been proposed as a promising means of improving the efficacy of radiotherapy against glioblastoma (GBM); however, the underlying mechanisms remain to be fully clarified. Here, UTMD was shown to induce ferroptosis, an iron-dependent form of regulated cell death, in ionizing radiation (IR)-treated GL261 and 1016B cells, as evidenced by decreased cell viability, glutathione, and glutathione peroxidase 4 levels, and increased total reactive oxygen species (ROS), lipid ROS, iron/Fe2+, malondialdehyde contents, acyl-CoA synthetase long-chain family member 4 expression and cell death. Suppression of ferroptosis by ferrostatin-1 or deferoxamine abolished UTMD-induced radiosensitization in GBM cells, whereas blockade of apoptosis, autophagy, or necroptosis showed no significant effect. Conversely, induction of ferroptosis using erastin, RAS-selective lethal 3, and ferric ammonium citrate further promoted UTMD-mediated radiosensitivity of GBM cells. Mechanistically, UTMD markedly increased transferrin receptor 1 (TFR1) expression in IR-exposed GBM cells. TFR1 downregulation reversed UTMD-caused increase of intracellular Fe2+, subsequently inhibiting UTMD-induced ferroptosis and radiosensitivity of GBM cells, which were augmented by TFR1 overexpression. In GBM-bearing C57BL/6J and NOD-SCID mouse models, UTMD similarly upregulated TFR1 expression, triggered ferroptosis, and sensitized tumors to IR, and these effects were reversed by TFR1 knockdown. In conclusion, UTMD promoted the radiosensitivity of GBM partially by induction of TFR1-mediated ferroptosis, providing novel insights into the mechanism underlying UTMD-mediated radiosensitization.

PMID 42758222
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