Kidney Stones

Indole is an aromatic, heterocyclic, organic compound which widely distributed in the natural environment and can be produced by a variety of bacteria. Indole regulates various aspects of bacterial physiology, including spore formation, plasmid stability, resistance to drugs, biofilm formation, and virulence as an intercellular signal molecule.

2,8-Dihydroxyadenine is an endogenous metabolite that forms crystals in urine, leading to kidney stone formation and crystal deposition in the kidney. 2,8-Dihydroxyadenine induces crystal-induced tubular injury, inflammation, and fibrosis through crystal deposition in renal tubules, where crystals are excreted in urine, internalized by tubular epithelial cells, and transported to the interstitium. 2,8-Dihydroxyadenine upregulates CD44 expression near crystals, TNF-α signaling through NF-κB, and mTORC1 signaling, while inducing actin stress fiber formation and cytoskeletal remodeling. 2,8-Dihydroxyadenine downregulates epithelial-mesenchymal transition pathways and oxidative phosphorylation, and induces changes affecting inflammation, metabolism, and cell cycle regulation. 2,8-Dihydroxyadenine can be used in research on kidney disease, adenine phosphoribosyltransferase deficiency, and kidney stone disease.

Tripotassium hydroxycitrate is an orally active, multi-target, multi-bioactive organic acid. Tripotassium hydroxycitrate activates Nrf2 and its downstream molecule GPX4, increases glutathione levels, and thereby inhibits ferroptosis. Tripotassium hydroxycitrate activates the Nrf2/Keap1 and ACLY/NF-κB signaling pathways, upregulates the activities of antioxidant enzymes such as superoxide dismutase, reduces MDA content, thereby alleviating oxidative stress and renal tubular epithelial cell apoptosis, and improves pulmonary vascular and right ventricular remodeling. Tripotassium hydroxycitrate activates both the AMPK and mTORC1/S6K pathways, triggers the unfolded protein response, arrests the cancer cell cycle, and induces DNA fragmentation.

Benarthin is an orally active Pyroglutamyl peptidase inhibitor, THY1 inhibitor (with a K_d value of 5.13e-08 M) and competitive PGP-1 inhibitor (K_i = 1.2 µM). Benarthin is isolated from the culture broth of Streptomyces xanthophaeus MJ244-SF1. Benarthin disrupts the THY1-SFRP1 interaction, inhibits the activation of the GSK3α/β-β-catenin pathway, and reduces the upregulation of FASLG. Benarthin attenuates urothelial anoikis and reduces cell Apoptosis. Benarthin possesses iron-chelating activity. Benarthin maintains urothelial barrier integrity and blocks the pathological cascade of renal interstitial fibroblasts induced by HAP stimulation. Benarthin can be used in studies related to kidney stones.

Glyoxal (40% w/w in water) is an α-oxoaldehyde that inhibits Aldose Reductase, Glutathione Reductase, and NADPH synthase. Glyoxal (40% w/w in water) exhibits cytotoxicity, triggers oxidative stress, induces ROS accumulation, lipid peroxidation, mitochondrial membrane potential collapse, DNA damage, apoptosis, and massive production of advanced glycation end products (AGEs). Glyoxal (40% w/w in water) depletes glutathione and activates MAPK phosphorylation. It has lower toxicity as a fixative than paraformaldehyde (PFA) and serves as a precursor for the synthesis of oxalates and dietary carcinogens. Glyoxal (40% w/w in water) is suitable for research related to calcium oxalate kidney stones, diabetes, atherosclerosis, cardiovascular diseases, retinopathy, and cataracts.

Relaxin H3 (human) TFA is a relaxin peptide with anti-inflammatory, anti-apoptotic, anti-pyroptotic, anti-migratory, protective and anti-fibrotic activities. Relaxin H3 (human) TFA acts on RXFP1 to generate cAMP and reduce the levels of ATP and ROS. Relaxin H3 (human) TFA inhibits renal inflammatory pyroptosis (pyroptosis), NLRP3 inflammasome activation, caspase-1 activation, IL-1β/IL-18 secretion, collagen synthesis, TGF-β1 signaling pathway, Smad2 phosphorylation, myofibroblast differentiation, TIMP expression, and HRMEC migration. Relaxin H3 (human) TFA activates AMPK, upregulates MFN2 expression, improves mitochondrial quality control and membrane potential, inhibits apoptosis (apoptosis) and pyroptosis, restores retinal ultrastructure, and reverses excessive left ventricular collagen expression. Relaxin H3 (human) TFA can be used in studies related to kidney stones, nephrocalcinosis, diabetic cardiomyopathy, fibrotic cardiomyopathy, and diabetic retinopathy.

Relaxin H3 (human) is a relaxin peptide with anti-inflammatory, anti-apoptotic, anti-pyroptotic, anti-migratory, protective and anti-fibrotic activities. Relaxin H3 (human) acts on RXFP1 to generate cAMP and reduce the levels of ATP and ROS. Relaxin H3 (human) inhibits renal inflammatory pyroptosis (pyroptosis), NLRP3 inflammasome activation, caspase-1 activation, IL-1β/IL-18 secretion, collagen synthesis, TGF-β1 signaling pathway, Smad2 phosphorylation, myofibroblast differentiation, TIMP expression, and HRMEC migration. Relaxin H3 (human) activates AMPK, upregulates MFN2 expression, improves mitochondrial quality control and membrane potential, inhibits apoptosis (apoptosis) and pyroptosis, restores retinal ultrastructure, and reverses excessive left ventricular collagen expression. Relaxin H3 (human) can be used in studies related to kidney stones, nephrocalcinosis, diabetic cardiomyopathy, fibrotic cardiomyopathy, and diabetic retinopathy.