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Development Status

US Previously Marketed

2

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Primary Target

Muscarinic acetylcholine receptor M1

2

Muscarinic acetylcholine receptor M2

2

Muscarinic acetylcholine receptor M3

2

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Highest Phase

Approved

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Approval Year

1956

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Condition

Peptic ulcer

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Treatment Modality

Primary

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CNS Activity

CNS Non-penetrant

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Originator

Sanofi

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Substance Class

Chemical

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Code System

CAS

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DRUG BANK

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EPA CompTox

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EVMPD

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FDA UNII

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ATC Level 1

ALIMENTARY TRACT AND METABOLISM

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ATC Level 2

DRUGS FOR FUNCTIONAL GASTROINTESTINAL DISORDERS

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ATC Level 3

DRUGS FOR FUNCTIONAL BOWEL DISORDERS

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ATC Level 4

Synthetic anticholinergics, quaternary ammonium compounds

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Substance Form

Principal Form

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Salts, Hydrates, Esters, etc.

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Mepenzolate

ONW3LB39P7

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Status:

US Previously Marketed

First approved in 1956

Class (Stereo):

CHEMICAL (RACEMIC)

Targets:

Muscarinic acetylcholine receptor M3

Muscarinic acetylcholine receptor M2

Muscarinic acetylcholine receptor M1

Conditions:

Mepenzolate is a postganglionic parasympathetic inhibitor. It decreases gastric acid and pepsin secretion and suppresses spontaneous contractions of the colon. It specifically antagonizes muscarinic receptors. Mepenzolate is marketed under the brand ...

name CANTIL. CANTIL is indicated for use as adjunctive therapy in the treatment of peptic ulcer. It has not been shown to be effective in contributing to the healing of peptic ulcer, decreasing the rate of recurrence, or preventing complications.

Mepenzolate Bromide

APX8D32IX1

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Status:

US Previously Marketed

First approved in 1956

Class (Stereo):

CHEMICAL (RACEMIC)

Targets:

Muscarinic acetylcholine receptor M3

Muscarinic acetylcholine receptor M2

Muscarinic acetylcholine receptor M1

Conditions:

Mepenzolate is a postganglionic parasympathetic inhibitor. It decreases gastric acid and pepsin secretion and suppresses spontaneous contractions of the colon. It specifically antagonizes muscarinic receptors. Mepenzolate is marketed under the brand ...

name CANTIL. CANTIL is indicated for use as adjunctive therapy in the treatment of peptic ulcer. It has not been shown to be effective in contributing to the healing of peptic ulcer, decreasing the rate of recurrence, or preventing complications.

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