Hyperuricemia

Xanthine, a plant alkaloid found in tea, coffee, and cocoa, is a mild stimulant of the central nervous system. Xanthine also acts as an intermediate product on the pathway of purine degradation.

Uricase, Microorganism (Uox, Microorganism) is a uricase (urate oxidase) derived from Microorganism. Uricase, Microorganism converts uric acid into allantoin. The absence of Uricase in mammals causes kidney diseases resulting from uric acid accumulation. Uricase, Microorganism can be used for research on chronic refractory gout and hyperuricemia.

Ulodesine (BCX4208) is a purine nucleoside phosphorylase (PNP) inhibitor, with an IC₅₀ of 2.293 nM against human PNP, and low nanomolar IC₅₀ values against mouse, rat and monkey PNP. Ulodesine blocks the production of uric acid precursors, reduces serum uric acid levels, clears accumulated uric acid in the blood, and elevates the levels of purine nucleosides including guanosine. Ulodesine reduces the counts of total lymphocytes, T lymphocytes and lymphocyte subsets, inhibits the proliferation of cancer cells and activated lymphocytes, and enhances vaccine immune responses. Ulodesine can be used in research related to hyperuricemia and gout.

5-O-Methylvisammioside (4'-O-β-D-Glucosyl-5-O-methylvisamminol) is an orally active natural chromone glycoside and multiple biological activities. 5-O-Methylvisammioside inhibits ferroptosis by activating the Nrf2/HO-1 signaling axis. 5-O-Methylvisammioside alleviates intestinal barrier damage by inhibiting the ROS/NF-κB/NLRP3 pathway. 5-O-Methylvisammioside exerts a protective effect against acute liver injury by reducing ALT/AST, decreasing inflammatory infiltration, and inhibiting IκB-α phosphorylation and NF-κB nuclear translocation. 5-O-Methylvisammioside blocks the HMGB1/RAGE/MEK/ERK signaling axis to exert anti-tumor and anti-angiogenic effects. 5-O-Methylvisammioside improves depression-like behaviors by inhibiting Src kinase and the NF-κB pathway.

Uricase (Recombinant) (Uox (Recombinant)) is a uricase (urate oxidase). Uricase (Recombinant) converts uric acid into allantoin. The deficiency of Uricase in mammals causes kidney diseases resulting from uric acid accumulation. Uricase (Recombinant) can be used for research on chronic refractory gout and hyperuricemia.

Febuxostat 67M-1 is an active metabolite of Febuxostat (HY-14268). Febuxostat 67M-1 retains inhibitory activity against Xanthine Oxidase, but its plasma concentration is much lower than that of Febuxostat. Febuxostat 67M-1 can be used in the research of hyperuricemia.

URAT1-IN-16 is an orally active URAT1 inhibitor with an IC₅₀ value of 0.19 μM. URAT1-IN-16 also functions as an NLRP3 inflammasome pathway inhibitor by effectively suppressing mature IL-1β secretion (IC₅₀ = 2.52 μM). URAT1-IN-16 exhibits remarkable serum uric acid-lowering and anti-inflammatory activities in vivo, and can be used for hyperuricemia and gout research.

URAT1/GLUT9-IN-2 is a selective, orally active URAT1/GLUT9 inhibitor, with an IC₅₀ of 2.81 μM against URAT1 and an IC₅₀ of 12.53 μM against GLUT9. URAT1/GLUT9-IN-2 reduces serum uric acid levels and protects renal function. URAT1/GLUT9-IN-2 can be used in research related to hyperuricemia and hyperuricemic nephropathy.

Xanthine oxidoreductase-IN-6 (Compound 4) is an orally active xanthine oxidoreductase (XOR) inhibitor with an IC₅₀ of 170 nM. Xanthine oxidoreductase-IN-6 can block the final step of uric acid biosynthesis and lower serum uric acid levels. Xanthine oxidoreductase-IN-6 also shows Cytochrome P450 3A4 (CYP3A4) inhibitory activity. Xanthine oxidoreductase-IN-6 can be used for the research of hyperuricemia.

Azaleatin is an orally active inhibitor of hQC, NS2B-NS3 protease and E. coli β-glucuronidase, with IC₅₀ values of 1.1 μM, 38.00 μg/mL and 0.57 μM, respectively. Azaleatin inhibits the activities of NF-κB, MyD88, JAK1, TLR4, STAT3, IL-1β, IL-6, COX-2, TNF-α and β-glucuronidase, blocks pro-inflammatory signaling pathways, reduces the levels of ROS, MDA and uric acid, elevates the levels of GPx, GSR, GST, SOD, CAT, HO-1 and GSH, scavenges free radicals and exerts reducing capacity. Azaleatin inhibits the expression of pro-apoptotic proteins Bax, Caspase-9 and Caspase-3, and upregulates the expression of anti-apoptotic protein Bcl-2. Azaleatin reduces the levels of cardiac injury markers, restores cardiac histological structure, inhibits Aβ aggregation, dengue protease activity, hepatic stellate cell proliferation and cancer cell growth, and also exhibits antibacterial activity. Azaleatin can be used in studies related to subchronic cardiotoxicity, Alzheimer's disease, dengue fever, hyperuricemia, liver fibrosis, gastric cancer and bacterial infections.

Xininurad is a potent orally active URAT1 inhibitor with an IC₅₀ of 7.17 nM. Xininurad inhibits URAT1 activity to reduce serum uric acid levels and increase urinary uric acid excretion. Xininurad can be used for the research of hyperuricemia and gout.

Procyanidin B2 3′-O-gallate (B2-3′-G), isolated from Rhodiola crenulata extracts, is a potent xanthine oxidase (XO) inhibitor (IC₅₀ = 24.24 μM, K_i = 6.16 μM). Procyanidin B2 3′-O-gallate has antioxidant activity and reduces the formation of UV-induced α-tocopheroxyl. Procyanidin B2 3′-O-gallate can be used for hyperuricemia and gout research.

Uricase, candida utilis (Uox, candida utilis) is a uricase (urate oxidase) derived from Candida utilis. Uricase, candida utilis converts uric acid into allantoin. The absence of Uricase in mammals causes kidney diseases resulting from uric acid accumulation. Uricase, candida utilis can be used for research on chronic refractory gout and hyperuricemia.

Benziodarone is a potent inhibitor of S-arylglutathione transferase enzyme system. Benziodarone catalyzes BSP conjugation with GSH. Benziodarone inhibits biliary excretion of synthetic BSP-GSH conjugates.

URAT1/GLUT9-IN-3 is an orally active URAT1/GLUT9 dual inhibitor with IC₅₀ values of 4.01 and 1.60 μM. URAT1/GLUT9-IN-3 inhibits URAT1-mediated uric acid uptake and GLUT9-mediated uric acid transport, reducing renal urate reabsorption. URAT1/GLUT9-IN-3 reduces serum uric acid levels in hyperuricemic mice. URAT1/GLUT9-IN-3 can be used for the researches of gout and hyperuricemia.

Xanthine oxidase-IN-23 (Compound BPF) is an orally active, reversible, mixed-type Xanthine oxidase inhibitor with an IC₅₀ of 3.33 μM. Xanthine oxidase-IN-23 directly binds to XOD in a reversible mixed-type manner to inhibit its catalytic activity. Xanthine oxidase-IN-23 upregulates ABCG2 and downregulates GLUT9 to promote renal urate excretion. Xanthine oxidase-IN-23 reduces serum urate levels and improves renal function in hyperuricemic mice. Xanthine oxidase-IN-23 can be used in the research of hyperuricemia.

Pantothenate kinase-IN-3 is an orally active PANK3-selective binder and CoA biosynthesis activator with a human PANK3 K_i of 9.1 nM, human PANK3 K_a of 1.8 nM, human PANK1β K_i of 113 nM, human PANK1β K_a of 23.4 nM, and oral effectiveness.Pantothenate kinase-IN-3 binds PANK3 via a water-mediated interaction between its sulfonamide NH and Gly193, elevates cellular, hepatic, and forebrain CoA levels, and shows improved metabolic stability in mouse and human microsomes.Pantothenate kinase-IN-3 has solubility properties favorable at pH 7.Pantothenate kinase-IN-3 can be used for the research of hepatic metabolic CoA deficiencies (acidemias).

PDE4-IN-33 is a phosphodiesterase 4 (PDE4) inhibitor. PDE4-IN-33 reduces uric acid levels. PDE4-IN-33 PDE4-IN-33 can be used for the research of hyperuricemia and gout.

Smilaxchinoside A is an orally active steroidal glycoside found in the roots of S. riparia. Smilaxchinoside A reduces serum uric acid levels and shows potent uricosuric activity. Smilaxchinoside A inhibits XOD activity and downregulates renal mURAT1 expression. Smilaxchinoside A can be used for the research of hyperuricemia.

Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease.