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6-CHLORO-3-INDOXYL PALMITATE - CAS 209347-96-6

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Category
Main Product
Product Name
6-CHLORO-3-INDOXYL PALMITATE
Catalog Number
209347-96-6
Synonyms
RARECHEM AH BS 0034;SALMON(TM)-PAL;6-CHLORO-3-INDOXYL PALMITATE
CAS Number
209347-96-6
Molecular Weight
406
Molecular Formula
C24H36ClNO2
COA
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MSDS
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Canonical SMILES
CCCCCCCCCCCCCCCC(=O)OC1=CNC2=C1C=CC(=C2)Cl
InChI
InChI=1S/C24H36ClNO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-24(27)28-23-19-26-22-18-20(25)16-17-21(22)23/h16-19,26H,2-15H2,1H3
InChIKey
GYQVOAOTWFXDDC-UHFFFAOYSA-N
Structure
CAS 209347-96-6 6-CHLORO-3-INDOXYL PALMITATE
Specification
Purity
95%
Appearance
Off-white to rose colored powder
Reference Reading
1.Hemophagocytic lymphohistiocytosis caused by systemic herpes simplex virus type 1 infection: Successful treatment with dexamethasone palmitate.
Otsubo K1, Fukumura A1, Hirayama M1, Morimoto T1, Kato M1, Mochizuki H1. Pediatr Int. 2016 Apr 14. doi: 10.1111/ped.12817. [Epub ahead of print]
Hemophagocytic lymphohistiocytosis (HLH) is a hyperinflammatory condition resulting from an uncontrolled and ineffective immune response. Here, we report a case of HLH caused by disseminated herpes simplex virus (HSV)-1 infection. The patient was initially treated with prednisolone and high-dose acyclovir. Although liver enzymes, coagulation abnormalities, and inflammatory markers were remarkably improved, the platelet count remained low. Prednisolone was therefore switched to dexamethasone palmitate. Thereafter, the platelet count normalized. Inflammatory markers normalized 30 days after admission and serum HSV-DNA became undetectable on day 41. The patient was discharged on day 91 and no developmental delay was evident at 7 months of age. These findings suggest that dexamethasone palmitate is effective for neonatal HLH.
2.Risperidone (depot) for schizophrenia.
Sampson S1, Hosalli P, Furtado VA, Davis JM. Cochrane Database Syst Rev. 2016 Apr 14;4:CD004161. [Epub ahead of print]
BACKGROUND: Risperidone is the first new generation antipsychotic drug made available in a long-acting injection formulation.
3.Astragaloside IV facilitates glucose transport in C2C12 myotubes through the IRS1/AKT pathway and suppresses the palmitate-induced activation of the IKK/IκBα pathway.
Zhu R1, Zheng J1, Chen L1, Gu B1, Huang S1. Int J Mol Med. 2016 Apr 11. doi: 10.3892/ijmm.2016.2555. [Epub ahead of print]
Astragaloside IV is a monomer isolated from Astragalus membranaceus (Fisch.) Bunge, which is one of the most widely used plant-derived drugs in traditional Chinese medicine for diabetes therapy. In the present study, we aimed to examine the effects of astragaloside IV on glucose in C2C12 myotubes and the underlying molecular mechanisms responsible for these effects. Four-day differentiated C2C12 myotubes were exposed to palmitate for 16 h in order to establish a model of insulin resistance and 3H glucose uptake, using 2-Deoxy‑D‑[1,2-3H(N)]-glucose (radiolabeled 2-DG), was detected. Astragaloside IV was added 2 h prior to palmitate exposure. The translocation of glucose transporter 4 (GLUT4) was evaluated by subcellular fractionation, and the expression of insulin signaling molecules such as insulin receptor β (IRβ), insulin receptor substrate (IRS)1/protein kinase B (AKT) and inhibitory κB kinase (IKK)/inhibitor-κBα (IκBα), which are associated with insulin signal transduction, were assessed in the basal or the insulin‑stimulated state using western blot analysis or RT-PCR.
4.Glutamine Modulates Macrophage Lipotoxicity.
He L1,2, Weber KJ3,4, Schilling JD5,6,7. Nutrients. 2016 Apr 12;8(4). pii: E215. doi: 10.3390/nu8040215.
Obesity and diabetes are associated with excessive inflammation and impaired wound healing. Increasing evidence suggests that macrophage dysfunction is responsible for these inflammatory defects. In the setting of excess nutrients, particularly dietary saturated fatty acids (SFAs), activated macrophages develop lysosome dysfunction, which triggers activation of the NLRP3 inflammasome and cell death. The molecular pathways that connect lipid stress to lysosome pathology are not well understood, but may represent a viable target for therapy. Glutamine uptake is increased in activated macrophages leading us to hypothesize that in the context of excess lipids glutamine metabolism could overwhelm the mitochondria and promote the accumulation of toxic metabolites. To investigate this question we assessed macrophage lipotoxicity in the absence of glutamine using LPS-activated peritoneal macrophages exposed to the SFA palmitate. We found that glutamine deficiency reduced lipid induced lysosome dysfunction, inflammasome activation, and cell death.
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