Prilocaine is a local anesthetic of the amino amide type first prepared by Claes Tegner and Nils Löfgren. In its injectable form, it is often used in dentistry. It is also often combined with lidocaine as a topical preparation for dermal anesthesia, for t + some more technical info. Chemically, prilocaine is an amide linked tertiary amine with formula C13H20N2O and a molecular weight of 220.31 g mol-1. It has a pKa near 7.9, moderate lipophilicity and roughly 50 to 60 percent protein binding, which together influence onset and duration. The principal pharmacologic action is reversible blockade of voltage gated sodium channels in peripheral nerves leading to loss of impulse conduction. Onset after infiltration or nerve block is typically within a few minutes and clinical duration is short to intermediate depending on dose, concentration, use of vasoconstrictor and the tissue treated. Prilocaine is metabolized primarily by hepatic and plasma amidases to yield metabolites including o toluidine, which under high dose or impaired clearance can cause methemoglobinemia. Typical formulations include 4 percent prilocaine plain for dental infiltration and combination creams with lidocaine in defined ratios for topical dermal anesthesia.
Parent: Prilocaine / Aniline
Parent: Prilocaine
Parent: Prilocaine
Parent: Prilocain
Parent: Prilocaine
Parent: Prilocaine
Parent: Prilocaine Hydrochloride / Prilocaine
Parent: Prilocaine
Typical quality control for prilocaine active pharmaceutical ingredient monitors related substances including N dealkylation products, hydrolysis products, the aromatic amine o toluidine, despropyl derivatives and process related impurities from synthesis such as unreacted anilines and O alkylation by products. Typical API and finished product specifications used in manufacturing and pharmacopeial monographs control individual related compounds generally at or below the 0.1 to 0.5 percent range by weight and total impurities below approximately 1.0 percent by weight, with particularly toxic species such as o toluidine often limited to low parts per million levels for safety, commonly specified at or below 0.05 percent by weight depending on regional regulatory requirements. Analytical methods for release and stability include HPLC with UV or MS detection and confirmatory GC MS for volatile or low level aromatic amines, with residual solvents and heavy metal limits applied per standard guidance.
Prilocaine is used to produce local anesthesia for minor surgical, dental and dermatologic procedures. Injectable solutions are commonly used for local infiltration and nerve blocks in dentistry and surgery, while topical mixtures with lidocaine are used to numb skin prior to needle insertion or superficial procedures.
Both are amino amide local anesthetics that block voltage gated sodium channels, but they differ in potency, onset, metabolism and side effect profile. Prilocaine tends to have slightly lower systemic toxicity at equivalent doses and a similar to slightly faster onset, while lidocaine is more widely used and has a broader range of formulations. Prilocaine is metabolized to o toluidine which can induce methemoglobinemia at high doses, a risk less associated with lidocaine.
Prilocaine undergoes hepatic and plasma amidase mediated hydrolysis and N dealkylation to form several metabolites; a principal metabolite is o toluidine, an aromatic amine that can oxidize hemoglobin to methemoglobin. Metabolism is rapid, contributing to a relatively short systemic half life; renal excretion clears polar metabolites.
Duration depends on route, concentration, dose and presence of vasoconstrictor. Typical infiltration or peripheral block durations are in the short to intermediate range, often from about 30 minutes up to 2 hours for soft tissue, with pulpal anesthesia in dental applications commonly shorter. Addition of a vasoconstrictor will prolong local effect by reducing systemic absorption.
