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Metabolites of Dihydro-alpha-ergocryptine are predicted with biotransformer.

Dihydrocodeine is an opioid analgesic agent used for the management of pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Dihydrocodeine is a semi-synthetic opioid analgesic. Dihydrocodeine is metabolized to dihydromorphine, a highly active metabolite with a high affinity for mu opioid receptors. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, dihydromorphine exerts its principal pharmacologic effects on the central nervous system. Dihydromorphine binds on pre-synaptic mu opioid receptors. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA. Less GABA leads to disinhibition of dopamine cell firing in the spinal cord pain transmission neurons. This leads to less pain signaling and analgesia. Opioids close N-type voltage-operated calcium channels and open calcium-dependent inwardly rectifying potassium channels. This results in hyperpolarization and reduced neuronal excitability. The inhibition of A delta and C pain fibres in the dorsal horn of the spinal cord is very important as it slows the signaling of pain into the spinal cord. Possible opioid related side effects include, but are not limited to, drowsiness, nausea, headache, dry mouth, constipation, difficulty passing urine, and mild euphoria.

Dihydrocodeine is an opioid analgesic agent used for the management of pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Dihydrocodeine is a semi-synthetic opioid analgesic. Dihydrocodeine is metabolized to dihydromorphine, a highly active metabolite with a high affinity for mu opioid receptors. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, dihydromorphine exerts its principal pharmacologic effects on the central nervous system. Dihydromorphine binds on pre-synaptic mu opioid receptors. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA is decreased. Less GABA leads to disinhibition of dopamine cell firing in the spinal cord pain transmission neurons. This leads to less pain signaling and analgesia. Opioids close N-type voltage-operated calcium channels and open calcium-dependent inwardly rectifying potassium channels. This results in hyperpolarization and reduced neuronal excitability. The inhibition of A delta and C pain fibres in the dorsal horn of the spinal cord is very important as it slows the signaling of pain into the spinal cord. Possible opioid related side effects include, but are not limited to, drowsiness, nausea, headache, dry mouth, constipation, difficulty passing urine, and mild euphoria.

Metabolites of Dihydroergocornine are predicted with biotransformer.

Metabolites of Dihydroergocristine are predicted with biotransformer.