iron chelating agent

1-2g SQ over 10-12hrs daily

iron chelating agent

20mg/kg/daily

- acetlyation of the cyclooxygenase active site

-acts on the hypothalmus

- anti-inflammatory

- low degree of analgesia

- uricosuric, only in high doses

- metabolized by N-deacylation to salicylic acid

- active metabolite of aspirin

- metabolized by glycine conjugation to salicyluric acid

- metabolized by p-hydroxylation to gentisic acid

- found in oil of wintergreen

-toxic when taken internally

- mainly used in topical preparations like Ben-Gay

- a salol (covalently bonded combination of 2 drugs)

- cleaved in the GI tract to salicylic acid and phenol

- salicylate class with a nuclear substitution

- twice as potent as aspirin

- less GI toxicity

- salicylate class with a nuclear substitution

- 3 times more potent than aspirin

- antipyretic effects

- causes methemoglobinemia, which may result in cyanosis and death

analgesic

antipyretic

not an anti-inflammatory drug

- reacts with the epoxide

- protects the liver from the arylation intermediate

- becomes particularly toxic in an acute overdose

- metabolized by N-deacetylation and glucuronidation

- a metabolite of acetaminophen that occurs when the normal pathway is staturated

- reacts rapidly with GSH, causing a complete depletion of glutathione

results in dramatic hepatotoxicity

- ethyl ether derivative of acetaminophen

- more toxic

- immediately O-dealkylated to acetaminophen

- no longer marketed

- a salol

- metabolized to acetaminophen and salicylic acid

- pyrazolinone

- antipyretic and analgesic

- can cause sedation

- pyrazoline: one of the double bonds is saturated

- pyrazolidine: both are saturated

- more potent than antipyrene

- can cause agranulocytosis

- removed from the market

- anti-inflammatory

- quite toxic

- pka near 4.5

- causes blood dyscrasias, no longer marketed

-active metabolite of phenylbutazone

- very toxic, off market

- strong electron leaving group

- pKa 2.8

- less anti-inflammatory agent, used as an uricosuric in the treatment of gout

- trifluoromethyl group in the 3 position

- NSAID, no analgesia

- methyl groups on the 2 and 3 position

- many side effects

- lower potency

2nd position: Cl

3rd position: CH3

6th position: Cl

- 150 x more potent than aspirin

- the halogens prevent the free rotation of the rings, making it a better fit for the receptor.

- potent NSAID

- carboxyl moiety is termed alpha

- pka 4.5

- arylacetic acid

- pKa 4.7

- a indene isostere: double bond replaces nitrogen in the indole ring

- remains in cis position, which is optimal for receptor activity

- metabolite sulfide form is also active

NSAID equal to ibuprofen

- lower risk of GI upset

- arylpropionic acid

- alpha methyl group, giving it stereochemistry

- S isomer is active

- R isomer is inactive

- contains arylalkanoic acid and anthranilic acid classes

- NSAID

- drug contains no acidic fuctional groups

- converted by oxidation to the arylacetic acid 6MNA

- causes less GI erosion

- long half life

- pyranocarboxylic acid

- NSAID

- oxicam

long half life

- enolic hydroxyl group, pha 4.3

- arthritis treatment

- disease modifying agents for rheumatoid diseases

- alter factors pertaining the etiology of disease rather than alleviaing disease- induced inflammation

- mimics the action of prostaglandins PGE1

- protects the stomach from damage caused by chronic use of NSAIDs

- used in acute attacks in gout

- 1mg q2hrs until pain subsides

- increases the renal secretion of uric acid

- it also inhibits the renal excretion of penicillin, increasing its half life

- competitive inhibitor of xanthine oxidase

- its converted to alloxanthine which also inhibits the enzyme

- inhibits the metabolism of 6-mercaptopurine (cancer drug)