Indomethacin


CAS No. : 53-86-1

(Synonyms: Indometacin)

53-86-1
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Cat. No. : HY-14397
M.Wt: 357.79
Formula: C19H16ClNO4
Purity: >98 %
Solubility: DMSO : 100 mg/mL (ultrasonic);H2O : < 0.1 mg/mL;Ethanol : 12.5 mg/mL (ultrasonic)
Introduction of 53-86-1 :

Indomethacin (Indometacin) is a potent, orally active COX1/2 inhibitor with IC50 values of 18 nM and 26 nM for COX-1 and COX-2, respectively. Indomethacin has anticancer activity and anti-infective activity. Indomethacin can be used for cancer, inflammation and viral infection research[1][2][3]. IC50 & Target:IC50: 18 nM (Human COX-1, in CHO cells), 26 nM (Human COX-2, in CHO cells)[1] In Vitro:Indomethacin (Indometacin) (0-150 μM; 24 hours; 3LL-D122 cells) has anticancer activity in vitro[2].
Indomethacin (Indometacin) (0-1000 μM) protects the host cells from damage caused by the virus through activates PKR, resulting in elF2α phosphorylation, and in turn shutting of translation of viral protein and inhibiting replication of the virus (IC50=2μM)[3]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Indomethacin can be used to induce gastric ulcer models. After oral administration, the drug is absorbed rapidly and completely, although there are interindividual and intraindividual variations. Typically, the plasma peak concentration (2-3 μg/mL) is reached within 1-2 hours. However, coadministration with food reduces and delays the peak concentration without affecting the total absorption. At therapeutic concentrations, 90% of Indomethacin is bound to albumin in the plasma[4].

Induction of gastric ulceration[5][6]
Background
Indomethacin can cause gastric ulceration by various mechanisms, including injury through inhibition of prostaglandin (PG) synthesis, reduction in local blood flow, regional irritation, and inhibition of tissue regeneration.
Specific Modeling Methods
Rat: albino Sprague-Dawley • male • adult (period: 2 weeks)
Administration: 100 mg/kg • p.o. • single dose
Note
(1) All animals fasted 24 h before drug administration.
(2) Indomethacin was dissolved in saline with 5% NaOH.
Modeling Indicators
Gastric tissue macroscopic alterations: Showed prominent mucosal folds and severe erosion, pronounced ulceration and bleeding foci in the gastric mucosa.
Histopathological changes: Showed severe erosion of the mucosa, reaching down to the lamina muscularis; observed hemorrhagic infiltration, edema in the submucosa, and severe hyperemia of the vessels.
Molecular changes: Showed intense Tnf-α expression.
Biochemical changes: Increased MDA, TOS levels, reduced TAS levels, CAT and GPx activities and GSH levels.
Correlated Product(s): Indomethacin sodium hydrate (HY-14397A)
Opposite Product(s): Carnosic acid (HY-N0644)

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