1. Immunology/Inflammation
    Apoptosis
  2. COX
    Apoptosis
  3. Diclofenac potassium

Diclofenac potassium 

Cat. No.: HY-15038 Purity: >98.0%
Handling Instructions

Diclofenac potassium is a potent and nonselective anti-inflammatory agent, acts as a COX inhibitor, with IC50s of 4 and 1.3 nM for human COX-1 and COX-2 in CHO cells, and 5.1 and 0.84 μM for ovine COX-1 and COX-2, respectively. Diclofenac potassium induces apoptosis of neural stem cells (NSCs) via the activation of the caspase cascade.

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Diclofenac potassium Chemical Structure

Diclofenac potassium Chemical Structure

CAS No. : 15307-81-0

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Based on 6 publication(s) in Google Scholar

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Description

Diclofenac potassium is a potent and nonselective anti-inflammatory agent, acts as a COX inhibitor, with IC50s of 4 and 1.3 nM for human COX-1 and COX-2 in CHO cells[1], and 5.1 and 0.84 μM for ovine COX-1 and COX-2, respectively[2]. Diclofenac potassium induces apoptosis of neural stem cells (NSCs) via the activation of the caspase cascade[3].

IC50 & Target[1][2]

Human COX-2

1.3 nM (IC50, in CHO cells)

Human COX-1

4 nM (IC50, in CHO cells)

Ovine COX-2

0.84 nM (IC50)

Ovine COX-1

5.1 nM (IC50)

In Vitro

Diclofenac effectively blocks COX-1 mediated prostanoid production from U937 cell microsomes, with an IC50 of 7±3 nM[1].
Diclofenac (1-60 μM; 1 day) induces neural stem cells (NSCs)death in a concentration-dependent manner[3].
Diclofenac (10-60 μM; 6 hours) increases the expression of cleaved (activated) caspase-3[3].

Cell Viability Assay[3]

Cell Line: Neural stem cells (NSCs)
Concentration: 1, 3, 10, 30, 60 μM
Incubation Time: 1 day
Result: Induction of cell death was concentration-dependent and the effect was not saturated at a concentration of up to 60 μM.

Western Blot Analysis[3]

Cell Line: Neural stem cells (NSCs)
Concentration: 10, 30 or 60 μM
Incubation Time: 6 hours
Result: The activation of caspase-3 was increased in a concentration-dependent manner.
In Vivo

Diclofenac (3 mg/kg, b.i.d., for 5 days) significantly increases faecal 51Cr excretion in rats, and such effect is also observed in squirrel monkeys after administrated of 1 mg/kg twice daily for 4 days[1].
Diclofenac (10 mg/kg; administered via oral route just prior to induction of inflammation) shows in vivo anti-inflammatory activity in Wistar rats[1].

Animal Model: Male Sprague-Dawley rats (150±200 g)[1]
Dosage: 3 mg/kg
Administration: Oral administration, b.i.d., for 5 days
Result: Resulted in a significant increase in faecal 51Cr excretion.
Animal Model: Wistar rats (150-175 g) bearing Formalin-induced rat foot paw edema model[2]
Dosage: 10 mg/kg
Administration: Administered via oral route just prior to induction of inflammation
Result: Showed in vivo anti-inflammatory activity (% edema inhibition=29.2, 1 h; 22.2, 3 h; 20, 6 h).
Molecular Weight

334.24

Formula

C₁₄H₁₀Cl₂KNO₂

CAS No.

15307-81-0

SMILES

O=C(O[K])CC1=CC=CC=C1NC2=C(Cl)C=CC=C2Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
References
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Keywords:

DiclofenacCOXApoptosisCyclooxygenaseanti-inflammatoryCOX-1COX-2CHOovineneuralstemcellsNSCscaspasecascadeInhibitorinhibitorinhibit

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Diclofenac potassium
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HY-15038
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