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Description Phenylpropanolamine has been withdrawn in Canada and the United States. In November 2000, the Food and Drug

Administration (FDA) issued a public health advisory against the use of the drug.

Pharmacology

Indication For the treatment of nasal congestion, control of urinary incontinence, priapism and obesity.

Pharmacodynamics Phenylpropanolamine (PPA), a sympathomimetic agent structurally similar to pseudoephedrine, is used to treat

nasal congestion. Phenylpropanolamine is found in appetite suppressant formulations and with guaifenesinin in

cough-cold formulations. In 2000, the FDA requested that all drug companies discontinue marketing products

containing phenylpropanolamine, due to an increased risk of hemorrhagic stroke in women who used

phenylpropanolamine.

Mechanism of

action

Phenylpropanolamine acts directly on alpha- and, to a lesser degree, beta-adrenergic receptors in the mucosa of th

respiratory tract. Stimulation of alpha-adrenergic receptors produces vasoconstriction, reduces tissue hyperemia,

edema, and nasal congestion, and increases nasal airway patency. PPA indirectly stimulates beta-receptors,

producing tachycardia and a positive inotropic effect.

Absorption Reduced bioavailability (about 38%) from gastrointestinal tract because of first pass metabolism by monoamine

oxidase in the stomach and liver.



NAME CHLORPHENAMINE

Accession Number DB01114 (APRD00001, DB09440)

Type Small Molecule

Groups Approved

Description A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used

in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less

drowsiness and sedation than promethazine. [PubChem]

Pharmacology

Indication For the treatment of rhinitis, urticaria, allergy, common cold, asthma and hay fever.

Pharmacodynamics In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils.Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to

cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once

released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H1



receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction.

Histamine also increases vascular permeability and potentiates pain. Chlorpheniramine, is a histamine H1 antagoni

(or more correctly, an inverse histamine agonist) of the alkylamine class. It competes with histamine for the normal

H1

-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provideseffective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper

respiratory allergies.

Mechanism of

action

Chlorpheniramine binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which

subsequently leads to temporary relief of the negative symptoms brought on by histamine.

Absorption Well absorbed in the gastrointestinal tract.

NAME METHYLPREDNISOLONE

Accession Number DB00959 (APRD00342)

Type Small Molecule

Groups Approved



Description A prednisolone derivative with similar anti-inflammatory action

Pharmacology

Indication Adjunctive therapy for short-term administration in rheumatoid arthritis.

Pharmacodynamics Methylprednisolone and its derivatives, methylprednisolone sodium succinate and methylprednisolone acetate, are

synthetic glucocorticoids used as antiinflammatory or immunosuppressive agents.

Mechanism of

action

Unbound glucocorticoids cross cell membranes and bind with high affinity to specific cytoplasmic receptors,

modifying transcription and protein synthesis. By this mechanism, glucocorticoids can inhibit leukocyte infiltration at

the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune

responses. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory

proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and

leukotrienes.

Absorption Oral bioavailability 80-99%

Name Acetaminophen



Accession Number DB00316 (APRD00252)

Type Small Molecule

Groups Approved

Description Acetaminophen, also known as paracetamol, is commonly used for its analgesic and antipyretic

effects. Its therapeutic effects are similar to salicylates, but it lacks anti-inflammatory, antiplatelet,

and gastric ulcerative effects

Indication For temporary relief of fever, minor aches, and pains.

Pharmacodynamics Acetaminophen (USAN) or Paracetamol (INN) is a widely used analgesic and antipyretic drug that

is used for the relief of fever, headaches, and other minor aches and pains. It is a major ingredient

in numerous cold and flu medications and many prescription analgesics. It is extremely safe in

standard doses, but because of its wide availability, deliberate or accidental overdoses are not

uncommon. Acetaminophen, unlike other common analgesics such as aspirin and ibuprofen, has

no anti-inflammatory properties or effects on platelet function, and it is not a member of the class

of drugs known as non-steroidal anti-inflammatory drugs or NSAIDs. At therapeutic doses

acetaminophen does not irritate the lining of the stomach nor affect blood coagulation, kidney

function, or the fetal ductus arteriosus (as NSAIDs can). Like NSAIDs and unlike opioid analgesics,

acetaminophen does not cause euphoria or alter mood in any way. Acetaminophen and NSAIDs



have the benefit of being completely free of problems with addiction, dependence, tolerance and

withdrawal. Acetaminophen is used on its own or in combination with pseudoephedrine,

dextromethorphan, chlorpheniramine, diphenhydramine, doxylamine, codeine, hydrocodone, or

oxycodone.

Mechanism of

action

Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting

both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin

(PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral

tissues and, thus, has no peripheral anti-inflammatory affects. While aspirin acts as an irreversible

inhibitor of COX and directly blocks the enzyme's active site, studies have found that

acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of

peroxides. This might explain why acetaminophen is effective in the central nervous system and in

endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies

also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme

that is different from the known variants COX-1 and COX-2. This enzyme is now referred to as

COX-3. Its exact mechanism of action is still poorly understood, but future research may provide

further insight into how it works. The antipyretic properties of acetaminophen are likely due to

direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral

vasodilation, sweating and hence heat dissipation.

Absorption Rapid and almost complete

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