presentation is based on mainly the chemistry of aspirin,A little bit introduction about nsaid is also here.The uses,doses and side effects are also in these presentation.

2. Non steroidal anti inflammatory drugs
Classification
Mechanism of action
Aspirin
Synthesis of Aspirin
SAR of Aspirin
Uses
Doses
Adverse Effect
Reference

3. These are a group of drugs which have an anti pyretic , anti-
inflammatory and analgesic effect .
They do not depress CNS.
They do not produce physical dependence
They act primarily on peripheral pain mechanisms but also in
the CNS to raise pain threshold.
They are commonly employed over the counter drugs (OTC).
They are also known as nonnarcotic , nonopioid, or aspirin like
analgesics.

4. Nonselective COX inhibitors: Preferential COX-2
inhibitors:
1. Salicylates :- Aspirin Nimesulide , Diclofenac ,
2. Propionic acid derivatives:-Ibuprofen , Naproxen Aceclofenac
3. Fenamate:-Mephenamic acid.
4. Enolic acid derivatives:-Piroxicam
5. Acetic aid derivatives:-Indomethacin
6. Pyrazolone derivatives:-Phenylbutazone.
Selective COX 2 inhibitors: Analgesic-antipyretics with poor
antiinflammatory action:
Celecoxib , Etoricoxib 1. Paraaminophenol derivatives:- Paracetamol
Paracoxib 2. Pyrazolone derivatives:-Metamizole
3. Benzoxazocine derivatives:-Neofam

5. Mainly by blocking of
Prostaglandins synthesis.
Cycloxygenase-1 & Cycloxygenase-2
Produce from Arachidonic acid.
Most NSAIDs inhibit COX-1
NSAIDs inhibit COX-2 nonselectively.
But now some selective COX-2
inhibitors have been produced.

6. Pharmacokinetic data
Bioavailability 80–100%
Protein binding 80–90%
Biological half-life Dose-dependent; 2–3 hours
for low doses, 15–30 hours
for large doses.
Excretion Urine (80–100%), sweat,
saliva, feces
Chemical data
Formula C9H8O4
Molecular mass 180.157 g/mol
Physical data
Density 1.40 g/cm
3
Melting point 135 °C (275 °F)
Boiling point 140 °C (284 °F) (decomposes)
Solubility in water 3 mg/mL (20 °C)

7. Mechanism Of Action as Analgesic :

10. Aspirin
Aspirin is synthesized by the acetylation of salicylic
acid using acetic anhydride or acetyl chloride.

12. CONTINUED…
1) Substitution on carboxyl groups may affect the potency and
toxicity.
2) Reducing the acidity of the –COOH, retains the analgesic
action of salicylic acid , but it is devoid of the anti-
inflammatory properties.
3) Placing the phenolic hydroxyl group , meta or para to the
carboxyl group abolishes the activity .
4) Substitution of halogen atoms on the aromatic ring enhances
potency and toxicity.
5) Substitution of aromatic rings at the 5 position of salicylic
acid increases anti-inflammatory activity.

13. U S E S
As an analgesic
As an anti- pyretic
To cure acute rheumatic fever
Rheumatoid arthritis
Osteoarthritis

14. Symptoms/Therapeutic use Dose
For the relief of minor aches &
mild to moderate pain
325-650 mg every
4 hrs.
For arthritis 3.2 gm - 6 gm/day
For reducing the risk of ischemia 1.3 gm /day
For myocardial infraction
prophylaxis
40 mg – 325 gm
/day

15. Side effects – Nausea, vomiting,
peptic ulcer.
Hypersensitivity and idiosyncrasy –
rashes, fixed drug erruption,
urticaria.
Acute salicylate poisoning-
vomiting, dehydration,
halucination, convulsion.

16.  T.L.Lemke,D.A.Williams,Foye’s principles of Medicinal Chemistry,6th
Edition,Wolters Kluwer(India),Nonsteroidal anti-inflammatory drugs,
Chemistry of Aspirin,Page No-965-969.
 D.Sriram,P.Yogeeswari,Medicinal Chemistry,2nd Edition,Pearson,
Antipyretics & Non-steroidal Anti-Inflammatory drugs,Salicyclic Acid
Derivatives,Page no-230-231.
 K.D.Tripathi,Essentials of Medical Pharmacology,7th edition,Jaypee,
Nonsteroidal anti-inflammatory drugs,The Salicylates,Page no-179-184.