Carbomer

UNDER REVIEW (September 2016)

Mechanism of Action:
Ocular lubricant.

 

Aciclovir

UNDER REVIEW (September 2016)

Mechanism of Action:
A partial nucleoside analogue with the sugar ring replaced by an open-chain structure. Converted to aciclo-GTP (by thymidine kinase) which is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times higher affinity to viral than cellular polymerase reducing toxicity towards human cells. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination. It has also been shown that the viral enzymes cannot remove acyclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase.

Lecture and CAL materials:

Neostigmine

UNDER REVIEW (September 2016)

Mechanism of Action:

Neostigmine is a reversible, medium-acting anticholinesterase drug (therapeutic effect up to 4 hours). Anticholinesterases competitively inhibit the action of acetylcholinesterase (AChE), which destroys the neurotransmitter acetylcholine following its release from cholinergic nerve endings. By interfering with the breakdown of acetylcholine, neostigmine indirectly (via action of ACh) stimulates both nicotinic and muscarinic receptors. Because neostigmine increases the effective concentration of acetylcholine, it causes such body changes as contraction of the pupils, increased activity of intestinal muscles, and increased secretion by the salivary and sweat glands. Neostigmine is a parasympathomimetic, ie it mimics the effects of stimulation of the parasympathetic nervous system.

Lecture and CAL materials:

Latanoprost

UNDER REVIEW (September 2016)

Mechanism of Actions:

Latanoprost, a derivative of the endogenous chemical, prostaglandin F2-alpha, is used for the treatment of glaucoma. Glaucoma is a condition in which the pressure exerted by the liquid within the eyeball (the aqueous humor) is too great. The high pressure damages the optic nerve at the back of the eye. The damage interferes with the ability of the nerve to transmit visual images from the eye to the brain and thus can lead to blindness. Latanoprost, by binding to a specific receptor for prostaglandin, increases the flow of aqueous humor out of the eye, thereby reducing the pressure within the eye and reducing the risk of nerve damage and blindness.

Lecture and CAL materials:

Timolol

UNDER REVIEW (September 2016)

Mechanism of Action:

Timolol is a beta-adrenergic blocking agent (beta adrenoceptor antagonist). Used in glaucoma as a topical intraocular pressure [IOP] reducing drug. It acts by blocking actions of the sympathetic nervous system, specifically it is an antagonist at beta-adrenoceptors on the ciliary processes, which results in a reduction of aqeuous secretions.

Lecture and CAL materials:

Tropicamide

UNDER REVIEW (September 2016)

Mechanism of Action:

Muscarinic receptor antagonist (non-selective for the various subtypes). Muscarinic AChRs are seven-transmembrane G-protein-coupled receptors (7TM GPCRs) which are activated by the endogenous neurotransmitter, acetylcholine. They are generally associated with the parasympathetic nervous system, and also cholinergic transmission in the CNS. Actions of parasympathetic nerves include smooth muscle contraction, increased glandular secretion and pupil constriction. It is also important in accommodation for seeing near objects – by control of ciliary muscles, the contraction of which decreases the focal distance of the lens. Muscarinic antagonists (also known as parasympatholytics) block these actions.

Lecture and CAL materials:

Chloramphenicol

UNDER REVIEW (April 2017)

Mechanism of Action:

Inhibits protein synthesis in bacteria. Chloramphenicol stops bacterial growth by inhibiting the enzyme peptidyl transferase, which inhibits ribosomal activity and protein synthesis by preventing the binding of amino acyl-tRNA to the A site on the 50S subunit. Resistance to chloramphenicol is conferred by the cat-gene. This gene codes for an enzyme called “chloramphenicol acetyltransferase” which inactivates chloramphenicol by covalently linking one or two acetyl groups, derived from acetyl-S-coenzyme A, to the hydroxyl groups on the chloramphenicol molecule. The acetylation prevents chloramphenicol from binding to the ribosome.

Lecture and CAL materials:

Pilocarpine

Mechanism of Action

Pilocarpine is a cholinomimetic drug that mimics the effects of acetylcholine which is produced by nerve cells. Acetylcholine is the major neurotransmitter in postganglionic neurones of the paratympathetic nervous system and is responsible for causing the salivary glands to make saliva, the lacrimal glands to make tears, and the pupils to constrict. A naturally occurring alkaloid obtained from plants of the genus Pilocarpus (family Rutaceae). By mimicking the effects of acetylcholine, pilocarpine acts as a stimulant of the parasympathetic nervous system. It promotes the flow of saliva and urine and increases perspiration. Because it increases the outflow of fluid from the eye, reduces the pressure within the eye, and causes the pupil to contract, the drug is used to treat some types of glaucoma.