Details of Drug-Drug Interaction
| Drug General Information (ID: DDIG9ASEMH) | |||||||||
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| Drug Name | Guanidine | Drug Info | Solifenacin | Drug Info | |||||
| Drug Type | Small molecule | Small molecule | |||||||
| Therapeutic Class | Cholinergic Muscle Stimulants | Antispasmodics | |||||||
| Structure | |||||||||
| Mechanism of Guanidine-Solifenacin Interaction (Severity Level: Moderate) | |||||||||
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| Antagonize the effect of cholinergic agents Click to Show/Hide Mechanism Graph | |||||||||
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| Drug Name | Guanidine | Solifenacin | |||||||
| Mechanism |
Cholinergic effects Acetylcholinesterase Inhibitor |
Anticholinergic effects Muscarinic acetylcholine receptor Antagonist |
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| Key Mechanism Factor 1 | |||||||||
| Factor Name | Acetylcholinesterase |
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Structure
Sequence
MRPPQCLLHTPSLASPLLLLLLWLLGGGVGAEGREDAELLVTVRGGRLRGIRLKTPGGPVSAFLGIPFAEPPMGPRRFLPPEPKQPWSGVVDATTFQSVCYQYVDTLYPGFEGTEMWNPNRELSEDCLYLNVWTPYPRPTSPTPVLVWIYGGGFYSGASSLDVYDGRFLVQAERTVLVSMNYRVGAFGFLALPGSREAPGNVGLLDQRLALQWVQENVAAFGGDPTSVTLFGESAGAASVGMHLLSPPSRGLFHRAVLQSGAPNGPWATVGMGEARRRATQLAHLVGCPPGGTGGNDTELVACLRTRPAQVLVNHEWHVLPQESVFRFSFVPVVDGDFLSDTPEALINAGDFHGLQVLVGVVKDEGSYFLVYGAPGFSKDNESLISRAEFLAGVRVGVPQVSDLAAEAVVLHYTDWLHPEDPARLREALSDVVGDHNVVCPVAQLAGRLAAQGARVYAYVFEHRASTLSWPLWMGVPHGYEIEFIFGIPLDPSRNYTAEEKIFAQRLMRYWANFARTGDPNEPRDPKAPQWPPYTAGAQQYVSLDLRPLEVRRGLRAQACAFWNRFLPKLLSATDTLDEAERQWKAEFHRWSSYMVHWKNQFDHYSKQDRCSDL
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| Gene Name | ACHE | ||||||||
| Uniprot ID | ACES_HUMAN | ||||||||
| KEGG Pathway | hsa:43 | ||||||||
| Protein Family | Type-B carboxylesterase/lipase family | ||||||||
| Protein Function |
Hydrolyzes rapidly the acetylcholine neurotransmitter released into the synaptic cleft allowing to terminate the signal transduction at the neuromuscular junction. Role in neuronal apoptosis.
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| Key Mechanism Factor 2 | |||||||||
| Factor Name | Muscarinic acetylcholine receptor M | Structure Sequence | |||||||
| Protein Family | G-protein coupled receptor 1 family | ||||||||
| Protein Function |
The muscarinic acetylcholine receptor mediates various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Primary transducing effect is Pi turnover.
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| Mechanism Description |
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| Recommended Action | |||||||||
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| Management | Agents with potent anticholinergic activity should preferably be avoided in patients receiving cholinergic skeletal muscle stimulants. If concurrent use is necessary, patients treated for myasthenia gravis should be monitored for potential exacerbation of symptoms. | ||||||||
| References | |||||||||||||||||||
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| 1 | Product Information. Mestinon (pyridostigmine). ICN Pharmaceuticals Inc, Cost Mesa, CA. | ||||||||||||||||||

