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NON-STEROIDAL ANTI-INFLAMETORYAGENT
Presented by Presented to
MOHD ATEEK ( Assistant Prof.)
SAURABH KUMAR Mr. RAVI KUMAR
GAURAV VERMA
NARENDRA KASAUDHAN
Introduction
 NSAIDs are the drug which used to treat
inflammation, pain, fever, and specific use
treatment of headache, arthritis, menstrual
cramps.cramps.
 These are also called non narcotic analgesic.
 They reduce dull aching pain but not usefull in
vsceral pain.
Classification
 1. Nonselective COX inhibitor
 Salicylate – Aspirin
 Propionic Acid Derivative – Ibuprofen
 2. Preferential COX-2 inhibitor
 Diclofenac, Nimesulide, Aceclofenac Diclofenac, Nimesulide, Aceclofenac
 3. Selective COX -2 inhibitor
 Celecoxib, Rofecoxip
 4. Analgesic – Antipyretic with poor
antiinflammatory Action
 Paracetamol, Metamizol, Propiphenazone,
Salicylates -Aspirin
 For nearly 200 years aspirin use for clinical purpose. Earlier it
was derived from willow bark but now it is synthesised.
 Mechanism of Action
 Aspirin is non-selective and irreversibly inhibits both forms Aspirin is non-selective and irreversibly inhibits both forms
(but is weakly more selective for COX-1). It does so by
acetylating the hydroxyl of a serine residue. Normally COX
produces prostaglandins, most of which are pro-inflammatory,
and thromboxanes, which promote clotting.
 Pharmacokinetic
 Metabolism in liver and bind 80-90% in blood and excreted
through urine
PharmacologicalAction
 Anti-inflammatory Action
 Analgesic Action
 Antipyretic Action
 Metabolic Effect Metabolic Effect
 Effect of Blood
 Endocrine Effect
 Gastrointestinal Effect
 CVS
 Use-
 Analgesic
 Antipyretic
 Osteoarthritis
 Post-Myocardial Infarction Post-Myocardial Infarction
 Adverse Effect-
 GIT Toxicity
 Salicylism
 Hypersensitivity
 Pregnancy
Propionic acid Derivative-Ibuprofen
 It have anti platelet effect .
 Mechanism of Action
 It inhibit cyclooxygenase enzyme involved in prostaglandin &
theomboxane bsynthesis via the arachidonic acid pathway.
 Pharmacokinetic Pharmacokinetic
 It bind to 90-99% plasma protien , metabolise in the liver , excreat
through 95%
 Use
 Dental pain
 Osteoarthritis
 Breast cancer
 Surgery
ArylAceticAcid Deerivatives-Diclofenac
 It have anti- pyretic, analgesic effect
 Mechanism of Action
 It inhibit leukocyte migration, COX-1 & COX-2
 It inhibit the synthesis of protaglandin . It inhibit the synthesis of protaglandin .
 It shows anti pyretic action via act on hypothalamus.
 Pharmacokinetic
 It bind to more than 99% ,metabolised in the liver exreated through
urine 60% bile duct 40%.
 Use
 Pain ,osteoarthritis, kidney stone, menstrual pain, cancer
Para-Aminophenol Derevative -PCM
 Mechanism of Action
 It inhibit the COX-1,COX-2, & COX-3 enzyme involved in the
synthisis of protaglandin.
 Pharmacokinetic Pharmacokinetic
 It bind 10-25%, metabolised in the liver ,excretion through urine
85-90%.
 Use
 fever,headche, osteoarthritis
 Adverse effct
 asthama kidney cancer, liver damage
Non-Steroidal antiinflammatory Drug Pharmacology By Saurabh Kumar

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Non-Steroidal antiinflammatory Drug Pharmacology By Saurabh Kumar

  • 1. NON-STEROIDAL ANTI-INFLAMETORYAGENT Presented by Presented to MOHD ATEEK ( Assistant Prof.) SAURABH KUMAR Mr. RAVI KUMAR GAURAV VERMA NARENDRA KASAUDHAN
  • 2. Introduction  NSAIDs are the drug which used to treat inflammation, pain, fever, and specific use treatment of headache, arthritis, menstrual cramps.cramps.  These are also called non narcotic analgesic.  They reduce dull aching pain but not usefull in vsceral pain.
  • 3.
  • 4. Classification  1. Nonselective COX inhibitor  Salicylate – Aspirin  Propionic Acid Derivative – Ibuprofen  2. Preferential COX-2 inhibitor  Diclofenac, Nimesulide, Aceclofenac Diclofenac, Nimesulide, Aceclofenac  3. Selective COX -2 inhibitor  Celecoxib, Rofecoxip  4. Analgesic – Antipyretic with poor antiinflammatory Action  Paracetamol, Metamizol, Propiphenazone,
  • 5. Salicylates -Aspirin  For nearly 200 years aspirin use for clinical purpose. Earlier it was derived from willow bark but now it is synthesised.  Mechanism of Action  Aspirin is non-selective and irreversibly inhibits both forms Aspirin is non-selective and irreversibly inhibits both forms (but is weakly more selective for COX-1). It does so by acetylating the hydroxyl of a serine residue. Normally COX produces prostaglandins, most of which are pro-inflammatory, and thromboxanes, which promote clotting.  Pharmacokinetic  Metabolism in liver and bind 80-90% in blood and excreted through urine
  • 6. PharmacologicalAction  Anti-inflammatory Action  Analgesic Action  Antipyretic Action  Metabolic Effect Metabolic Effect  Effect of Blood  Endocrine Effect  Gastrointestinal Effect  CVS
  • 7.  Use-  Analgesic  Antipyretic  Osteoarthritis  Post-Myocardial Infarction Post-Myocardial Infarction  Adverse Effect-  GIT Toxicity  Salicylism  Hypersensitivity  Pregnancy
  • 8. Propionic acid Derivative-Ibuprofen  It have anti platelet effect .  Mechanism of Action  It inhibit cyclooxygenase enzyme involved in prostaglandin & theomboxane bsynthesis via the arachidonic acid pathway.  Pharmacokinetic Pharmacokinetic  It bind to 90-99% plasma protien , metabolise in the liver , excreat through 95%  Use  Dental pain  Osteoarthritis  Breast cancer  Surgery
  • 9. ArylAceticAcid Deerivatives-Diclofenac  It have anti- pyretic, analgesic effect  Mechanism of Action  It inhibit leukocyte migration, COX-1 & COX-2  It inhibit the synthesis of protaglandin . It inhibit the synthesis of protaglandin .  It shows anti pyretic action via act on hypothalamus.  Pharmacokinetic  It bind to more than 99% ,metabolised in the liver exreated through urine 60% bile duct 40%.  Use  Pain ,osteoarthritis, kidney stone, menstrual pain, cancer
  • 10. Para-Aminophenol Derevative -PCM  Mechanism of Action  It inhibit the COX-1,COX-2, & COX-3 enzyme involved in the synthisis of protaglandin.  Pharmacokinetic Pharmacokinetic  It bind 10-25%, metabolised in the liver ,excretion through urine 85-90%.  Use  fever,headche, osteoarthritis  Adverse effct  asthama kidney cancer, liver damage