(-)-Epicatechin - CAS 490-46-0
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
(-)-Epicatechin
Catalog Number:
490-46-0
Synonyms:
(-)-Epicatechol; Epicatechin; epi-Catechin
CAS Number:
490-46-0
Description:
(−)-Epicatechin is a 2R,3R stereoisomer of catechin and is a naturally occurring flavanol. It is a powerful antioxidant and could inhibit cyclooxygenase.
Molecular Weight:
290.27
Molecular Formula:
C15H14O6
COA:
Inquire
MSDS:
Inquire
Targets:
Others
Chemical Structure
CAS 490-46-0 (-)-Epicatechin

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Reference Reading


1.Vitamin A or E and a catechin synergize as vaccine adjuvant to enhance immune responses in mice by induction of early IL-15 but not IL-1β responses.
Patel S1, Akalkotkar A1, Bivona JJ 3rd1, Lee JY2, Park YK2, Yu M1, Colpitts SL3, Vajdy M1. Immunology. 2016 May 2. doi: 10.1111/imm.12614. [Epub ahead of print]
Vitamins A and E and select flavonoids in the family of catechins are well-defined small molecules that if proven to possess immunomodulatory properties, hold promise as vaccine adjuvants and various therapies. In an effort to determine the in vivo immunomodulatory properties of these molecules, we found that while mucosal and systemic vaccinations with a recombinant HIV-1BaL gp120 with either a catechin, epigallo catechin gallate (EGCG) or pro vitamin A (retinyl palmitate) alone in a vegetable oil in water emulsion (OWE) suppressed antigen-specific responses, the combination of EGCG and vitamin A or E in OWE (Nutritive Immune-enhancing Delivery System, NIDS) synergistically enhanced adaptive B, and CD4+ and CD8+ T cell responses, following induction of relatively low local and systemic innate TNFα, IL-6, and IL-17, but relatively high levels of early systemic IL-15 responses. For induction of adaptive IFNγ and TNFα responses by CD4+ and CD8+ T cells, the adjuvant effect of NIDS was dependent on both IL-15 and its receptor.
2.Mortality reduction among persons with type 2 diabetes: (-)-Epicatechin as add-on therapy to metformin?
Moreno-Ulloa A1, Moreno-Ulloa J2. Med Hypotheses. 2016 Jun;91:86-9. doi: 10.1016/j.mehy.2016.04.018. Epub 2016 Apr 12.
Diabetes has become a worldwide epidemic, and is growing at a rapid rate with drastic projections for developing countries. Mexico occupies the ninth place worldwide for type 2 diabetes prevalence, and in the foreseeable future, it is expected rise to the seventh place. Myocardial infarction is the most common cause of death in these patients. Although several drugs are approved for the treatment of type 2 diabetes that reduce factors associated with myocardial infarction, an excess risk of death is still present. In this regard, the American Diabetes Association recommends metformin (oral glucose lowering drug) as the first-line therapy in type 2 diabetic subjects, based on its amply confirmed positive metabolic effects; however, its capacity to reduce cardiovascular mortality in type 2 diabetic subjects is inconclusive. Thus, mortality reduction in these patients has been an elusive goal, and is therefore, imperative to evaluate new pharmacological interventions that may favorably impact mortality in these individuals.
3.Green tea catechin prevents hypoxia/reperfusion-evoked oxidative stress-regulated autophagy-activated apoptosis and cell death in microglial cells.
Chen CM, Wu CT, Yang TH, Chang YA, Sheu ML, Liu SH. J Agric Food Chem. 2016 May 4. [Epub ahead of print]
Defective activation and proliferation in microglial cells has been suggested to be associated with the increase of cerebral ischemia/reperfusion injury. We investigated the protection and molecular mechanism of green tea catechin on hypoxia/reperfusion-induced microglial cell injury in vitro. Microglial cells were cultured in hypoxia condition (O2 < 1%) and then re-incubated to the complete normal culture medium (reperfusion). Hypoxia/reperfusion obviously decreased cell viability and induced apoptosis in microglial cells, but not in neuronal cells. Catechin significantly inhibited the hypoxia/reperfusion-induced decreased cell viability and increased reactive oxygen species (ROS) and apoptosis in microglia. The administration of both PI3K/Akt inhibitor LY294002 and mTOR inhibitor rapamycin demonstrated that Akt/mTOR-regulated autophagy was involved in the hypoxia/reperfusion-induced microglia apoptosis/death. Catechin upregulated the Akt and mTOR phosphorylation and inhibited the hypoxia/reperfusion-induced autophagy in microglia.