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CAS:66827-12-1
Molecular Formula:CH11AlMg3O12
Brief Introduction
Aluminum magnesium addition does not play a therapeutic role simply by neutralizing gastric acid. It inhibits the guaranteed hydrolysis of pepsin by reducing acid ions and absorbing pepsin, prevents further damage of pepsin to gastric mucosa when gastric mucosa fails, and selectively absorbs cholic acid and hemolytic soft phospholipids, which plays a certain role in gastric ulcer caused by bile reflux.
Metkephamid; Metkefamide; Unii-Mnl20Fxh9Y; Mnl20Fxh9Y
Brief Introduction
Is a synthetic opioid pentapeptide and derivative of [Met]enkephalin with the amino acid sequence Tyr-D-Ala-Gly-Phe-(N-Me)-Met-NH2. It behaves as a potent agonist of the δ- and μ-opioid receptors with roughly equipotent affinity, and also has similarly high affinity as well as subtype-selectivity for the κ3-opioid receptor. Despite its peptidic nature, upon systemic administration, metkefamide rapidly penetrates the blood-brain-barrier and disperses into the central nervous system where it produces potent, centrally-mediated analgesic effects, of which have been shown to be dependent on activity at both the μ- and δ-opioid receptors. In addition, on account of modifications to the N- and C-terminals, metkefamide is highly stable against proteolytic degradation relative to many other opioid peptides. As an example, while its parent peptide, [Met]enkephalin, has an in vivo half-life of merely seconds, metkefamide has a half-life of nearly 60 minutes, and upon intramuscular administration, has been shown to provide pain relief that lasts for hours. Likely on account of its δ-opioid activity, clinical trials have found metkefamide to possess less of a tendency for producing many of the undesirable side effects usually associated with conventional opioids such as respiratory depression, tolerance, and physical dependence. However, it has been shown to cause some additional side effects that are considered unusual for standard opioid analgesics like sensations of heaviness in the extremities and nasal congestion—though these were not considered to be particularly distressing—and it has also been shown to raise the seizure threshold in animals. In any case, clinical development was not further pursued after phase I clinical studies and metkefamide never reached the pharmaceutical market.
Brief Introduction
The molecular formula of MetkephaMide acetate is C31H44N6O8S.
CAS:67-07-2
Molecular Formula:C4H10N3O5P
Phosphocreatine; Creatine Phosphate; N-(N1-(Dihydroxyphosphinyl)Amidino)Sarcosine; Creatine Phosphate (Phosphocreatine); Creatine Phosphoric Acid; N-Methyl-N-Phosphonocarbamimidoyl-Glycin; N-Methyl-N-Phosphonocarbamimidoyl-Glycine; N-Phosphono-Kreatin
Brief Introduction
Phosphocreatine - or creatine phosphate - is the phosphorylated form of creatine. It is primarily found endogenously in the skeletal muscles of vertebrates where it serves a critical role as a rapidly acting energy buffer for muscle cell actions like contractions via its ability to regenerate adenosine triphosphate (ATP) from adenosine diphosphate (ADP).
CAS:67-73-2
Molecular Formula:C24H30F2O6
Ethyl O-Mesitylsulfonylacetohydroxamate; 6α,9α-Difluoro-11β,16α,17α,21-Tetrahydroxy-1,4-Pregnadiene-3,20-Dione; Fluocinonide; 6A,9A-Fifluoro-16A,17A-Isopropylidenedioxy-1,4-Pregnadiene-3,20-Dione
Brief Introduction
Fluocinolone Acetonide is the acetonide salt form of fluocinolone, a synthetic fluorinated corticosteroid with antiinflammatory, antipruritic and vasoconstrictive properties. Fluocinolone is a glucocorticoid receptor agonist that binds to cytoplasmic glucocorticoid receptors and subsequently translocates to the nucleus where it initiates the transcription of glucocorticoid-responsive genes such as lipocortins. Lipocortins inhibit phospholipase A2, thereby blocking the release of arachidonic acid from membrane phospholipids and preventing the synthesis of prostaglandins and leukotrienes, both are potent mediators of inflammation. Fluocinolone exerts its vasoconstrictive effect through inhibition of nitric oxide synthase, thereby blocking nitric oxide production and effectively diminishing the effect of nitric oxide on vascular smooth muscles leading to reduced blood flow.
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