bilirubin

Bilirubin conjugate is a stable, water-soluble ditaurate derivative of bilirubin meant to mimic endogenous bilirubin glucuronide derivatives. In vivo, bilirubin circulates in the plasma and is taken up by hepatocytes and conjugated to one or two glucuronic acids in a reaction catalyzed by UDP glucuronidase to form bilirubin mono or diglucuronide. This water-soluble form is then excreted from the liver in bile in the feces or is converted to urobilinogen and excreted in the urine. In addition to aiding in the disposal of heme, bilirubin and its conjugated derivatives have been shown to exhibit anti-oxidant and antimutagenic effects and to play a role in gut barrier function.

Bilirubin (Principal bile pigment) is a type of bile pigment, which is a metabolite of hemoglobin in the blood. Bilirubin has antimutagenic and antioxidant effects. Bilirubin is an important basis for clinical determination of jaundice, and is also an important indicator of liver function.

Bilirubin-d4 is the deuterated form of Bilirubin.

Bilirubin oxidase (BOD), a multi-copper oxidase, catalyzes the transformation of bilirubin into biliverdin while reducing molecular oxygen to water. This enzyme plays a role in porphyrin and chlorophyll metabolism and is extensively employed as an oxygen reduction catalyst in biochemical research [1].

Bilirubindiglucuronide is a metabolite of Bilirubin. Bilirubin diglucuronide can inhibit the MRP1/2-mediated, ATP-dependent transport of leukotriene C4 (LTC4) in membrane vesicles.

Urobilinogens comprise a mixture of bilirubin metabolites, including D-urobilinogen, L-urobilinogen (stercobilinogen), and i-urobilinogen (mesobilirubinogen). These compounds are produced from bilirubin by gut microbiota. In mice on a high-fat diet, the cecal concentrations of D-urobilinogen, L-urobilinogen, and i-urobilinogen are increased. Furthermore, elevated fecal levels of L-urobilinogen are inversely associated with reduced blood hemoglobin levels in patients with heterozygous β-thalassemia.

Lumirubin is a water-soluble photoproduct of bilirubin formed in vivo during phototherapy.

Biliverdin hydrochloride is a tetrapyrrole compound formed from the oxidation of heme, with potential antioxidant activity, involved in the biliverdin-bilirubin redox system.

Nitisinone-13C6is intended for use as an internal standard for the quantification of nitisinone by GC- or LC-MS. Nitisinone is an inhibitor of 4-hydroxyphenylpyruvate dioxygenase (HPPD), which converts 4-hydroxyphenylpyruvate (HPPA) to homogentisate in the tyrosine catabolic pathway.1Nitisinone increases urinary levels of HPPA and 4-hydroxyphenyllactate (HPLA) in rats when administered at a dose of 10 mg/kg. Nitisinone (3 mg/kg) prevents the neonatal lethality of fumarylacetoacetate hydrolase (FAH) deficiency in mice when administered to pregnant dams.2It exhibits hepatoprotective effects inFAH-/-mice, such as prevention of increases in plasma levels of aspartate serine aminotransferase (AST) and conjugated bilirubin, when administration is continued following birth at a dose of 1 mg/kg. Nitisinone (100 μg) decreases urinary excretion of homogentisate and increases urinary excretion of HPPA, HPLA, and 4-hydroxyphenylacetate in a mouse model of alkaptonuria induced by ethylnitrosourea.3Formulations containing nitisinone have been used in the treatment of hereditary tyrosinemia type 1 (HT-1). 1.Ellis, M.K., Whitfield, A.C., Gowans, L.A., et al.Inhibition of 4-hydroxyphenylpyruvate dioxygenase by 2-(2-nitro-4-trifluoromethylbenzoyl)-cyclohexane-1,3-dione and 2-(2-chloro-4-methanesulfonylbenzoyl)-cyclohexane-1,3-dioneToxicol. Appl. Pharmacol.133(1)12-19(1995) 2.Grompe, M., Lindstedt, S., al-Dhalimy, M., et al.Pharmacological correction of neonatal lethal hepatic dysfunction in a murine model of hereditary tyrosinaemia type INat. Genet.10(4)453-460(1995) 3.Suzuki, Y., Oda, K., Yoshikawa, Y., et al.A novel therapeutic trial of homogentisic aciduria in a murine model of alkaptonuriaJ. Hum. Genet.44(2)79-84(1999)

Gastrin-releasing peptide (GRP) is a neuropeptide that stimulates gastrin release. It binds to (Ki = 300 nM) and stimulates amylase secretion in rat pancreatic AR42J cells (EC50 = 0.3 nM). GRP increases proliferation of human liver carcinoma HepG2 and MHCC97H cells but does not affect the proliferation of normal HL-7702 liver cells at a concentration of 1 nM. In vivo, GRP (0.35 nmol/kg/h) increases both pancreatic exocrine secretion and pancreatic polypeptide (PP) release in rats. It dose-dependently stimulates gastrin, pancreatic amylase, lipase, bilirubin, and acid output and induces gallbladder contraction in humans when administered at doses ranging from 1 to 27 pmol/kg per hour.

Phycocyanobilin (PCB), a linear open-chain tetrapyrrole chromophore, is a bilirubin analog with anti-inflammatory and antioxidant activity for the study of neurological disorders such as Alzheimer's disease.

Biliverdin, produced through the oxidation of bilirubin, can also be synthesized through a non-protoporphyrin pathway in Corynebacterium glutamicum [1].

6-Hydroxy Etodolac, a metabolite of the non-steroidal anti-inflammatory drug (NSAID) and COX inhibitor etodolac, causes false positives in diazo diagnostic tests for urinary bilirubin.

UGT1A1-IN-1 (compound 2) acts as a non-competitive inhibitor of UGT1A1, effectively inhibiting the 1-O-glucuronidation process mediated by UGT1A1 with a Ki value of 5.02 μM. This compound binds to the same ligand-binding site on UGT1A1 as bilirubin and additionally functions as a 'turn-on' fluorescent probe substrate for UGT1A1 [1].

Biliverdin hydrochloride (Standard) is a reference standard for research and analysis in studies involving Biliverdin hydrochloride. Biliverdin hydrochloride is a tetrapyrrole compound formed from the oxidation of heme, with potential antioxidant activity, involved in the biliverdin-bilirubin redox system.

Stercobilinogen is a microbial metabolite of bilirubin found in the intestines. It is utilized in metabolic research.

i-Urobilinogen is a reduced metabolite of bilirubin that can be isolated from human feces. It exhibits the ability to scavenge DPPH free radicals.

Biliverdin dihydrochloride is a tetrapyrrolic pigment resulting from the degradation of heme. Heme is broken down by heme oxygenase into biliverdin, carbon monoxide, and iron. Subsequently, biliverdin is rapidly converted to bilirubin by biliverdin reductase. Biliverdin dihydrochloride exhibits antimutagenic, antioxidant, anti-inflammatory, and immunosuppressive properties.