Examples include:

Prilocaine hydrochloride and epinephrine (trade name Citanest Forte)
Lidocaine, bupivacaine, and epinephrine (recommended final concentrations of 0.5, 0.25, and 0.5%, respectively)
Iontocaine, consisting of lidocaine and epinephrine
Septocaine (trade name Septodont), a combination of articaine and epinephrineOne combination product of this type is used topically for surface anaesthesia, TAC (5-12% tetracaine,1/2000 (0.05%, 500 ppm, 1⁄2 per mille) adrenaline, 4 or 10% cocaine). Using LA with vasoconstrictor is safe in regions supplied by end arteries. The commonly held belief that LA with vasoconstrictor can cause necrosis in extremities such as the nose, ears, fingers, and toes (due to constriction of end arteries), is invalidated, since no case of necrosis has been reported since the introduction of commercial lidocaine with epinephrine in 1948. Ester group
Benzocaine
Chloroprocaine
Cocaine
Cyclomethycaine
Dimethocaine (Larocaine)
Piperocaine
Propoxycaine
Procaine (Novocaine)
Proparacaine
Tetracaine (Amethocaine)

Amide group
Articaine
Bupivacaine
Cinchocaine (Dibucaine)
Etidocaine
Levobupivacaine
Lidocaine (Lignocaine)
Mepivacaine
Prilocaine
Ropivacaine
Trimecaine

Naturally derived
Saxitoxin
Neosaxitoxin
Tetrodotoxin
Menthol
Eugenol
Cocaine
SpilantholMost naturally occurring local anesthetics with the exceptions of menthol, eugenol and cocaine are neurotoxins, and have the suffix -toxin in their names. Cocaine binds the intracellular side of the channels while saxitoxin, neosaxitoxin and tetrodotoxin bind to the extracellular side of sodium channels. History
In Peru, the ancient Incas are believed to have used the leaves of the coca plant as a local anaesthetic in addition to its stimulant properties. It was also used for slave payment and is thought to play a role in the subsequent destruction of Incas culture when Spaniards realized the effects of chewing the coca leaves and took advantage of it. Cocaine was first used as a local anesthetic in 1884.
A small amount of vitamin B6 is also excreted in the feces. This may be a combination of unabsorbed vitamin and what was synthesized by large intestine microbiota. Deficiency
Signs and symptoms
The classic clinical syndrome for vitamin B6 deficiency is a seborrhoeic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy (due to impaired sphingosine synthesis) and microcytic anemia (due to impaired heme synthesis).Less severe cases present with metabolic disease associated with insufficient activity of the coenzyme PLP. The most prominent of the lesions is due to impaired tryptophan–niacin conversion. This can be detected based on urinary excretion of xanthurenic acid after an oral tryptophan load. Vitamin B6 deficiency can also result in impaired transsulfuration of methionine to cysteine. The PLP-dependent transaminases and glycogen phosphorylase provide the vitamin with its role in gluconeogenesis, so deprivation of vitamin B6 results in impaired glucose tolerance. Diagnosis
The assessment of vitamin B6 status is essential, as the clinical signs and symptoms in less severe cases are not specific. The three biochemical tests most widely used are plasma PLP concentrations, the activation coefficient for the erythrocyte enzyme aspartate aminotransferase, and the urinary excretion of vitamin B6 degradation products, specifically urinary PA. Of these, plasma PLP is probably the best single measure, because it reflects tissue stores. Plasma PLP of less than 10 nmol/l is indicative of vitamin B6 deficiency.