Sulfisoxazole is a sulfonamide antibacterial antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfisoxazole acetyl in combination with erythromycin ethylsuccinate is used for treatment of ACUTE OTITIS MEDIA in children that is caused by susceptible strains of Haemophilus influenzae. Sulfisoxazole acetyl is a prodrug of sulfisoxazole. Acetyl group is added to make the drug poorly water soluble, and is hydrolyzed in vivo to the active drug. Sulfisoxazole and its acetylated metabolites are excreted primarily by the kidneys through glomerular filtration. Sulfisoxazole is a competitive inhibitor of the enzyme dihydropteroate synthetase. It inhibits bacterial synthesis of dihydrofolic acid by preventing the condensation of the pteridine with para-aminobenzoic acid (PABA), a substrate of the enzyme dihydropteroate synthetase. The inhibited reaction is necessary in these organisms for the synthesis of folic acid

N-Acetyltyrosine is an acetylated derivative of the amino acid L-tyrosine. Ordinary L-tyrosine is less stable and also less soluble in water, which may result in reduced bioavailability. Acetylation enhances the solubility and stability of certain amino acids. N-Acetyltyrosine is commonly used in place of tyrosine in parenteral nutrition. It converts to tyrosine and then can be used in neurotransmitter treatment as a precursor of cathecholamine. N-Acetyltyrosine supports brain function by supporting the synthesis of the catecholamines norepinephrine and dopamine (neurotransmitters). N-Acetyltyrosine supplements are used to improve memory and cognitive performance in humans while they are experiencing psychological stress.

ACETYL HEXAPEPTIDE-8 (ARGIRELINE®), a hexapeptide Ac-EEMQRR-NH2, is an anti-wrinkling agent. It significantly inhibits neurotransmitter release with a potency similar to that of botulinum toxin. ACETYL HEXAPEPTIDE-8 (ARGIRELINE®) is a mimic of the N-terminal end of SNAP-25 which competes with SNAP-25 for a position in the SNARE complex, thereby modulating its formation. If the SNARE complex is slightly destabilized, the vesicle can not release neurotransmitters efficiently and therefore muscle contraction is attenuated, preventing the formation of lines and wrinkles.