Butamirate (or brospamin) is a medicine used for the symptomatic treatment of non-productive (dry) cough. Butamirate is centrally acting cough suppressant which is neither chemically nor pharmacologically related to opium alkaloids. In addition to its antitussive effect, Butamirate also decreases the airway resistance. Butamirate is rapidly and completely absorbed after oral administration. Maximum concentration is reached within 9 hours with sustain release tablet. Butamirate is extremely protein bound and Plasma elimination half-life is about 13 hours. Butamirate is indicated in acute cough of any etiology, pre and post operative cough sedation for surgical procedure and bronchoscopy. Butamirate is well tolerated. In rare cases, skin rash, nausea, diarrhea, dizziness have been reported.They disappear after reduction of the dosage or discontinuation of the drug.

Butetamate is a cough suppressant. It exerts antispasmodic, bronchodilator and anticholinergic properties.

Fenbutrazate is a prodrug of phenmetrazine, a psychostimulant for the treatment of obesity. Fenbutrazate acts as an agonist of monoamine transportes upon conversion to the active metabolite. The drug is no longer marketed due to its addictive profile.

Oxeladin citrate is a cough suppressant, is a highly potent and effective drug used to treat all types of cough of various etiologies. Withdrawn from the Canadian, US, and UK markets in 1976 due to carcinogenicity. Oxeladine is a component of antitussive drug, Altussan, approved in Philippines.

Sodium phenylbutyrate is a salt of an aromatic fatty acid. The compound is used to treat urea cycle disorders, because its metabolites offer an alternative pathway to the urea cycle to allow excretion of excess nitrogen. Sodium phenylbutyrate is also a histone deacetylase inhibitor and chemical chaperone, leading respectively to research into its use as an anti-cancer agent and in protein misfolding diseases such as cystic fibrosis. It is used as adjunctive therapy for the management of chronic urea cycle disorders due to deficiencies in carbamylphosphate (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase. It is indicated in all neonatal- onset efficiency presenting within the first 28 days of life. Also indicated in patients with late-onset, presenting after the first month of life with a history of hyperammonemic encephalopathy. Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to phenylacetate. Phenylacetate is a metabolically active compound that conjugates with glutamine via acetylation to form phenylacetylglutamine. The kidneys then excrete Phenylacetylglutamine. PBA (phenylbutyric acid) is absorbed from the intestine and converted by way of β-oxidation to the active moiety, phenylacetic acid (PAA). PAA is conjugated with glutamine in the liver and kidney by way of N-acyl coenzyme A-l-glutamine N-acyltransferase to form phenylacetylglutamine (PAGN). Like urea, PAGN incorporates two waste nitrogens and is excreted in the urine. On a molar basis, it is comparable to urea (each containing two moles of nitrogen). Therefore, phenylacetylglutamine provides an alternate vehicle for waste nitrogen excretion.