Ethopropazine is an anticholinergic drug. Ethopropazine is an inhibitor of butyrylcholinesterase and non-selective muscarinic acetylcholine receptor antagonist. Ethopropazine has been used for the treatment of parkinsonism and drug-induced extrapyramidal reactions. Also It used for the symptomatic treatment of hepatolenticular degeneration and congenital athetosis.

Tropatepine is an anticholinergic drug. Intramuscular injections of tropatepine are used to counteract the extrapyramidal effects of neuroleptic drugs and for the treatment of Parkinson's disease. The drug is marketed in Europe under tradename Lepticur.

Bornaptine is a synthetic anticholinergic drug. The compound is a nonselective M1 and M4 antagonist and was shown to inhibit the negative inotropic response to carbachol in the isolated left atrium of the rat with pA2 of 7.27. Bornaprine is used for the treatment of symptoms of Parkinson's disease. A clinical trial showed the superiority of Bornaprine over placebo in reducing parkinsonian tremor. Bornaptine demonstrated positive results in localized hyperhidrosis.

Ethybenzatropine (Ponalid) is an anticholinergic and antihistaminergic drug. It was used as an antiparkinsonian agent. A significant increase in the duration of action of levodopa-induced improvement in parkinsonian symptoms was observed following the administration of ethybenzatropine. Ethybenzatropine also improved, or tended to improve the duration and seventy of onset and end-of-dose levodopa-induced dyskinesias. Thus when levodopa is administered together with etybenzatropine, its length of action on parkinsonian symptoms is prolonged.

Mazaticol is an anti-acetylcholine agent used in Japan for the treatment of Parkinson's syndrome.

Dexetimide is a potent central and peripheral anticholinergic agent. It has a high affinity for all subtypes of muscarinic receptor and a long duration action. It forms very stable complex with mAChR. Dexetimide was used for many years in Europe for the treatment of extrapyramidal disorders. Neuroleptic-induced parkinsonian symptoms are effectively controlled by dexetimide. It is a safe, potent, and long-acting antiparkinsonian agent.

Aturban (phenglutarimide) is a neuropsychiatric agent, was used as therapeutic drug for parkinsonism. Phenglutarimide hydrochloride possesses parasympatholytic activity and has been available as an antiparkinson agent since its preparation by Tagman, Sury & Hoffmann (1952). Phenglutarimide is a muscarinic acetylcholine receptor antagonist. There are three subtypes of enantiomers of phenglutarimide. The affinity of the enantiomers of phenglutarimide at three muscarinic receptor subtypes was examined in vitro using field-stimulated rabbit vas deferens (M1 receptors) and guinea pig atria (M2 alpha receptors) and ileum (M2 beta receptors). Extremely high stereoselectivity was observed and higher affinities (up to 6000-fold) were found for the (+)-S-enantiomer. The stereoselectivity ratios were different at the three subtypes, and the stereochemical demands made by the muscarinic receptors were most stringent at M1 receptors. (+)-(S)-Phenglutarimide was found to be a potent M1-selective antagonist (pA2 at M1 = 8.53). Its receptor selectivity profile is qualitatively similar to that of pirenzepine. (-)-(R)-Phenglutarimide showed no comparable discriminatory properties.

Piribedil is an antiparkinsonian agent which acts as D2 and D3 receptor agonist. In European countries and worldwide it is used as a monotherapy or in combination with dopatherapy for treatment of Parkinson's disease, cognitive impairment and obliterating arteriopathy.

Selegiline, also known as L-deprenyl, is a substituted phenethylamine, a selective, irreversible inhibitor of Type B monoamine oxidase. Selegiline is available in pill form under many brand names (Eldepryl, Carbex, Atapryl) and is used to reduce symptoms in early-stage Parkinson's disease. Selegiline delays the time point when the L-DOPA (levodopa) treatment becomes necessary from about 11 months to about 18 months after diagnosis, which is beneficial despite not being definitive evidence of neuroprotection. The rationale for adding selegiline to levodopa is to decrease the required dose of levodopa and thus reduce the motor complications of levodopa therapy. Selegiline is also delivered via a transdermal patch (brand name, Emsam) and in this form, Selegiline is used as a treatment for the major depressive disorder. Selegiline (brand name Anipryl) is also used (at extremely high dosages relative to humans) in veterinary medicine to treat the symptoms of Cushing's disease and cognitive dysfunction (Canine Cognitive Dysfunction) in dogs. Side effects of the pill form include, in decreasing order of frequency, nausea, hallucinations, confusion, depression, loss of balance, insomnia, increased involuntary movements, agitation, arrhythmia, slow heart rate, delusions, hypertension, new or increased angina pectoris, and syncope. The main side effects of the patch form for depression included application site reactions, insomnia, diarrhea, and sore throat.

Carbidopa is a competitive inhibitor of aromatic L-amino acid decarboxylase that does not cross the blood-brain barrier, is routinely administered with levodopa (LD) for the treatment of the symptoms of idiopathic Parkinson’s disease (paralysis agitans), postencephalitic parkinsonism, and symptomatic parkinsonism, which may follow injury to the nervous system by carbon monoxide intoxication and/or manganese intoxication. Current evidence indicates that symptoms of Parkinson’s disease are related to depletion of dopamine in the corpus striatum. Administration of dopamine is ineffective in the treatment of Parkinson’s disease apparently because it does not cross the blood-brain barrier. However, levodopa, the metabolic precursor of dopamine, does cross the blood- brain barrier, and presumably is converted to dopamine in the brain. When levodopa is administered orally it is rapidly decarboxylated to dopamine in extracerebral tissues so that only a small portion of a given dose is transported unchanged to the central nervous system. For this reason, large doses of levodopa are required for adequate therapeutic effect and these may often be accompanied by nausea and other adverse reactions, some of which are attributable to dopamine formed in extracerebral tissues. Carbidopa inhibits decarboxylation of peripheral levodopa. Carbidopa has not been demonstrated to have any overt pharmacodynamic actions in the recommended doses.