Verinurad (CAS: 1352792-74-5) stands as a pivotal pharmaceutical compound, representing a significant advancement in the treatment of conditions linked to elevated uric acid levels. This potent and selective uric acid transporter 1 (URAT1) inhibitor is drawing considerable attention for its promising therapeutic applications, primarily in managing hyperuricemia and gout, and increasingly, in related renal and cardiovascular conditions.

Gout is a debilitating metabolic disease triggered by persistently high serum uric acid (sUA) levels, leading to the painful deposition of urate crystals in joints. A crucial element in maintaining uric acid homeostasis is the URAT1 transporter, predominantly found in the kidneys. URAT1 is responsible for the reabsorption of approximately 90% of the urate filtered by the glomerulus back into the bloodstream. In patients with gout, reduced fractional excretion of uric acid often contributes to hyperuricemia, making the inhibition of URAT1 a highly effective strategy to enhance renal uric acid excretion and lower sUA levels.

Research has demonstrated Verinurad’s exceptional efficacy and specificity. In in vitro studies, it exhibits remarkable potency, inhibiting human URAT1 with an IC50 as low as 25 nM. Furthermore, its selectivity is pronounced, showing approximately 200-fold lower affinity for related transporters such as OAT4 and OAT1, thereby minimizing potential off-target effects. Clinical evaluations underscore this potency; a single 40 mg oral dose of Verinurad has been shown to reduce baseline sUA levels by up to 60% for a sustained period in healthy volunteers. Intriguingly, significant sUA reduction can be achieved even at doses as low as 5 mg, highlighting its powerful pharmacological profile.

The molecular pharmacology of Verinurad provides deeper insights into its mechanism of action. Its high-affinity interaction with URAT1 is critically dependent on specific amino acid residues, including Ser-35, Phe-365, Ile-481, and notably, Cys-32, a residue uniquely important for Verinurad among known inhibitors. These residues are located within the transporter channel, suggesting that Verinurad binds to a common site in the core of the transporter. This binding then competitively hinders the transit of uric acid through the substrate channel, effectively preventing its reabsorption. This detailed understanding of its molecular interactions solidifies Verinurad’s potential as a targeted therapeutic agent.

Beyond its primary indications for gout and asymptomatic hyperuricemia, Verinurad is also under evaluation for its potential benefits in patients with chronic kidney disease (CKD) and hyperuricemia, and heart failure. Clinical trials are exploring its effects on reducing the urinary albumin to creatinine ratio (UACR), an important marker in CKD progression. Its capacity to significantly lower sUA levels offers a multifaceted therapeutic approach, potentially mitigating risks associated with hyperuricemia in a broader patient population. As research continues, Verinurad is poised to become a cornerstone in the management of hyperuricemia and its related systemic complications.

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