Sildenafil citrate (CAS 171599-83-0) is a potent and selective inhibitor of phosphodiesterase type 5 (PDE5), widely used as a reference compound in cardiovascular, urological, and oncological research. The compound is orally active and extensively characterized across both preclinical and clinical settings. Enamine offers Sildenafil citrate as a high-purity screening sample for pharmacological and biochemical studies.
Sildenafil citrate molecular structure consists of a pyrazolopyrimidinone core with an ethoxyphenylsulfonyl-methylpiperazine substituent, forming a citrate salt with molecular formula C₂₈H₃₈N₆O₁₁S and molecular weight of 666.70 g/mol. The Sildenafil citrate chemical structure is well-characterized and widely referenced in medicinal chemistry literature. Researchers consult the Sildenafil citrate structure to understand PDE5 active site binding geometry and selectivity determinants. The Sildenafil citrate chemical structure diagram illustrates how the pyrazolopyrimidinone scaffold coordinates the catalytic zinc ion, while the sulfonylpiperazine group occupies a hydrophobic pocket. The compound is registered under CAS 171599-83-0.
Application of Sildenafil citrate
Sildenafil citrate is used as a reference PDE5 inhibitor in studies of cGMP-mediated smooth muscle relaxation, pulmonary arterial hypertension, and erectile dysfunction pharmacology. Beyond its primary applications, the compound is investigated in cancer biology - particularly in PDE5-overexpressing oral squamous cell carcinoma - as well as in models of heart failure, Raynaud's phenomenon, and uteroplacental blood flow regulation. Also known as PF-01000000, it serves as a standard comparator in PDE isoform profiling assays due to its well-defined selectivity profile.
In Vitro
Sildenafil citrate inhibits human PDE5 with an IC₅₀ of approximately 3–4 nM, showing more than 1000-fold selectivity over PDE3. In smooth muscle cell assays, PDE5 inhibition elevates intracellular cGMP levels and potentiates nitric oxide–mediated relaxation. The compound also stimulates sperm motility in vitro and demonstrates inhibitory activity against cyclase enzymes, supporting its use in reproductive and vascular biology studies.
In Vivo
In animal models, Sildenafil citrate produces dose-dependent vasodilation in pulmonary and penile vasculature, reducing vascular resistance and improving tissue perfusion. Studies in dogs confirm clinically relevant improvement in smooth muscle–related conditions following oral dosing. The Sildenafil citrate molecular structure diagram corresponds to a pharmacokinetic profile characterized by rapid oral absorption and broad tissue distribution, supporting translational use in multiple in vivo experimental designs.
Biochemical and Physiological Actions
Sildenafil citrate selectively inhibits PDE5, the enzyme responsible for cGMP hydrolysis in smooth muscle cells. This inhibition stabilizes cGMP levels, sustaining activation of protein kinase G and downstream phosphorylation cascades that promote smooth muscle relaxation and vasodilation. The compound does not inhibit PDE1, PDE2, or PDE3, and shows approximately 10-fold lower potency against PDE6, underpinning its tissue selectivity. At the cellular level, elevated cGMP also modulates apoptotic signaling in tumor cells overexpressing PDE5.
Features and Benefits of Sildenafil citrate
Sildenafil citrate (CAS 171599-83-0) provides a thoroughly validated pharmacological profile relevant across multiple research areas:
- sub-nanomolar PDE5 inhibition (IC₅₀ ~4 nM) with high selectivity over other PDE isoforms;
- well-characterized Sildenafil citrate structure enabling rational analog and combination study design;
- activity validated across cardiovascular, oncological, and reproductive biology models;
- extensive clinical and preclinical dataset available for translational reference.
When sourced as EBC-11287, the compound is provided with analytical quality control data for reliable use in biochemical and cell-based assays.
