Bilirubin CAS 635-65-4

Produced when old red blood cells are broken down in the liver, bilirubin CAS 635-65-4 is a yellowish substance that is found in bile, a fluid your liver produces to help digest food. Bilirubin CAS 635-65-4 is transported to the liver by a protein called albumin, where it becomes conjugated, becoming water-soluble so it can be removed from the body. A healthy liver can remove the majority of bilirubin CAS 635-65-4 from the body, through releasing it into the bloodstream where it is sent to be eventually excreted by other organs.

Antioxidant Activity
Bilirubin CAS 635-65-4 has powerful antioxidant activity and has been shown to be capable of protecting from 10,000 fold molar excess of hydrogen peroxide . Reduction of oxidant-related stress is the key mechanism behind the protective effects of bilirubin CAS 635-65-4 in the kidney, heart and brain, the three organs that are most commonly affected by ischemia/reperfusion during cardiac bypass, myocardial infarction, stroke and severe hypotension. Bilirubin CAS 635-65-4 has similar effects in preventing nitrosative injury that is induced by peroxynitrite, a potent oxidant that is formed by the combination of nitric oxide (NO) and the superoxide anion, as occurs during renal ischemia reperfusion injury .

Anti-inflammatory And Immunomodulatory
After these early studies, investigators began to discover that bilirubin CAS 635-65-4 has immunomodulatory effects, with particular focus on decreasing the release of damage associated molecular patterns (DAMPS) and IL-1 β by injured pancreatic islet cells, which are key initiators of the innate immune response after cell or organ transplantation . Through suppression of these early signals, bilirubin CAS 635-65-4 supplementation has even enabled the generation of tolerance to organ transplants, reducing apoptosis, and release of inflammatory mediators (IL-1 β, soluble intercellular adhesion molecule 1 [ICAM1], and monocyte chemoattractant protein 1 [MCP-1], eliminating the early signaling that leads to allo-recognition and acute or chronic graft rejection . Cytoprotective effects of bilirubin CAS 635-65-4 are enacted in many ways beyond its direct anti-oxidant activity, including the inhibition of pro-apoptotic genes (TNF-α, Fas, iNOS, Caspase-3,-8,-9, and p38MAPK) and upregulation of antiapoptotic genes (HO-1 and bcl-2) .

Cytoprotective Effects of Bilirubin
Protective effects of bilirubin CAS 635-65-4 occur at multiple levels on the pathway to apoptosis. This schematic depicts some of the demonstrated effects of bilirubin CAS 635-65-4 on transplanted pancreatic islet cells. (Rao, W.; Gilor, C.; Xu, F.; He, X.; Adin, C.A. Nano-Encapsulation of bilirubin CAS 635-65-4 in Pluronic F127–Chitosan Improves Uptake in β Cells and Increases Islet Viability and Function after Hypoxic Stress. Cell Transplant. 2017, 26, 1703–1715, doi:10.1177/0963689717735112.

Excellent Team
The company has hired senior experts and PhDs in the field of biochemical synthesis in China to lead the guidance, and has a leading core team consisting of senior engineer Zeng Fanrong with a master's degree and multiple undergraduate research and development personnel.

Quality Services
Team members possess multilingual skills and are able to adapt to the diverse needs of the international market, establishing stable cooperative relationships with global clients.

Quality Assurance
We produce merchandise of the highest possible standard. Possessing the technology and skills to reach the requirements of our clients, we ensure that the merchandise produced reflects our commitment to providing our clients with a fast, reliable and cost-effective service without compromising on quality.

Drug development involves a high failure rate as candidate small molecule drugs and biologics must be tested through an ascending pathway that begins with in vitro experiments, then pass through rodents and large animal models before entering human clinical trials. Since bilirubin CAS 635-65-4 is a natural molecule that exists in all eukaryotes, any positive or negative effects in human and animal models can be investigated through epidemiologic studies that relate serum bilirubin CAS 635-65-4 concentrations to health outcomes. In fact, a mutation in the gene for uridine diphosphate glucuronosyltranferase (UGT-1A), the enzyme responsible for conjugation of bilirubin, is prevalent in the human population and approximately 5–10% of the population have mildly elevated serum total bilirubin concentrations of 1–6 mg/dL (17–100 µM) due to a condition termed Gilbert's Syndrome . Patients with Gilbert's Syndrome have an insertion in the promoter region of the gene, leaving the gene functional, but causing reduction of gene transcription to ~20% of normal . Many patients with Gilbert's Syndrome can have concurrent genetic abnormalities affecting bilirubin CAS 635-65-4 metabolism at multiple levels, including the genes for heme oxygenase-1, and biliverdin reductase . An animal model for Gilbert's Syndrome has been identified in Gunn rats, providing a correlate for experimental studies of hyperbilirubinemia .

Decades of epidemiologic studies in people with Gilbert's Syndrome have shown that mild elevations in serum bilirubin CAS 635-65-4 concentrations cause a decreased risk for coronary artery disease, stroke, myocardial infarction and improve outcomes in organ transplantation, with virtually no pathologic effects noted in affected individuals Patients with the more rare Criggler-Najar Syndrome have a mutation in the coding section of the UDPGT1A1 gene that causes complete inactivity of the UGT-1A enzyme, resulting in serum bilirubin CAS 635-65-4 concentrations in the 20–45 mg/dL 425–765 µM) range . At this level, toxic effects of bilirubin are observed, including potentially fatal neurotoxicity prior to adulthood unless liver transplantation is performed . These observational studies have been extremely useful in providing much of the needed safety, dose response and efficacy studies in human beings that would be gleaned from clinical trials.