Tetracaine Other names: Amethocaine Amethocaine hydrochloride Tetracaine Tetracaine hydrochloride

Tetracaine is a local anaesthetic and is believed to act by blocking nerve conduction mainly by inhibiting sodium ion flux across the axon membrane.

Tetracaine achieves this by acting upon specific receptors that control gating mechanisms responsible for conductance changes in specialised proteinaceous sodium channels.

Blocking sodium ion flux prevents the setting up of an action potential in the nerve axon, thus preventing pain receptors signalling to the central nervous system.

Tetracaine additionally has vasodilatory effects, which commonly results in a localised erythema.

Tetracaine is a weak base (pK_a 8.5), therefore, significant changes in the rate of ionised lipid soluble drug uptake may occur with changes in the acid base balance.

The ester type ‘caine’ anaesthetics are rapidly metabolised in blood mainly by plasma pseudocholinesterase. A 3.33μM (1μg/ml) concentration of tetracaine was fully metabolised in human plasma within 20 seconds.

In vivo data has demonstrated that tetracaine gel is 15 ± 11% bioavailable when administered to intact normal skin, with a mean absorption and elimination half life of 1.23 ± 0.28 hours. Peak plasma levels of p-(n-butylamino) benzoic acid (BABA), the major metabolite of tetracaine are between 3-6 hours post dose.

In vitro studies have shown that tetracaine has a high affinity for melanin, therefore, differences in duration of action may be expected between deeply pigmented eyes and less pigmented eyes.

The primary site of metabolism for tetracaine is the plasma. Pseudocholinesterases in the plasma hydrolyse tetracaine to 4-aminobenzoic acid. Unmetabolised drug is excreted in the urine.

No adverse safety issues were detected during the development of this formulation. The active ingredient is well established in clinical ophthalmology.