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Pathways

PathWhiz ID Pathway Meta Data

PW146592

Pw146592 View Pathway
drug action

Levomenol Drug Metabolism Action Pathway

Homo sapiens

PW000654

Pw000654 View Pathway
drug action

Levomethadyl Acetate Action Action Pathway

Homo sapiens
Levomethadyl acetate (also known as LAAM) is a synthetic synthetic opioid analgesic with multiple actions quantitatively similar to those as morphine, the most prominent of which involve the central nervous system and organs composed of smooth muscle. However, levomethadyl acetate is more active and more toxic than morphine. Levomethadyl acetate can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of levomethadyl acetate will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Therefore, methadyl acetate can reduce nerve conduction and decrease neurotransmitter release; so that perception of pain signals can be blocked. Levomethadyl acetate can also open calcium-dependent inwardly rectifying potassium channels (OP1 receptor agonist) to reduce neuronal excitability as well as lead to hyperpolarization.

PW147017

Pw147017 View Pathway
metabolic

Levomethadyl Acetate Drug Metabolism Pathway

Homo sapiens

PW000614

Pw000614 View Pathway
drug metabolism

Levomethadyl Acetate Metabolism Pathway

Homo sapiens
Levomethadyl Acetate (also known as levacetylmethadol or levo-α-acetylmethadol) (LAAM), is a synthetic opioid structurally similar to methadone. It is an opioid agonist that has been used as an analgesic and to treat opioid dependence. Levomethadyl Acetate is metabolized by cytochrome P450 3A4 in two N-demethylation reactions to nor-levomethadyl acetate (nor-LAAM) and subsequently to dinor-levomethadyl acetate (dinor-LAAM).

PW132496

Pw132496 View Pathway
metabolic

Levomilnacipran Drug Metabolism

Homo sapiens
Levomilnacipran is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Levomilnacipran passes through the liver and is then excreted from the body mainly through the kidney.

PW145891

Pw145891 View Pathway
drug action

Levomilnacipran Drug Metabolism Action Pathway

Homo sapiens

PW128028

Pw128028 View Pathway
drug action

Levomilnacipran SNRI - Norepinephrine reuptake Inhibition Action Pathway

Homo sapiens
Levomilnacipran (the more active 1S, 2R - enantiomer of milnacipran) is a serotonin and norepinephrine reuptake inhibitor (SNRI). It is used in the management of major depressive disorder, generalized anxiety disorder, chronic musculoskeletal pain and diabetic peripheral neuropathy. It is generally believed that 5HT and NE participate in the modulation of endogenous analgesic mechanisms by way of the descending inhibitory pain pathways in the brain and spinal cord. Although the specific mechanism of action remains unclear, some studies have proposed that low levels of 5HT may be associated with increased sensitivity to pain - a condition that could subsequently be improved by milnacipran's capacity to enhance the presence of 5HT by inhibiting its reuptake via serotonin transporters at synaptic clefts. Furthermore, in the CNS it is also generally believed that NE released from descending pathways can mitigate pain sensations via eliciting inhibitory effects on alpha-2A-adrenoceptors on central terminals of primary afferent nociceptors, by direct alpha-2-adrenergic action on pain-relay neurons, and by alpha-1-adrenoceptor-mediated activation of inhibitory interneurons. Such NE pain mitigation is consequently also enhanced by milnacipran's ability to enhance the presence of NE by inhibiting its reuptake via norepinephrine transporters at synaptic clefts

PW127981

Pw127981 View Pathway
drug action

Levomilnacipran SNRI - Serotonin Reuptake Inhibition Action Pathway

Homo sapiens
Levomilnacipran (the more active 1S, 2R - enantiomer of milnacipran) is a serotonin and norepinephrine reuptake inhibitor (SNRI). It is used in the management of major depressive disorder, generalized anxiety disorder, chronic musculoskeletal pain and diabetic peripheral neuropathy. It is generally believed that 5HT and NE participate in the modulation of endogenous analgesic mechanisms by way of the descending inhibitory pain pathways in the brain and spinal cord. Although the specific mechanism of action remains unclear, some studies have proposed that low levels of 5HT may be associated with increased sensitivity to pain - a condition that could subsequently be improved by milnacipran's capacity to enhance the presence of 5HT by inhibiting its reuptake via serotonin transporters at synaptic clefts. Furthermore, in the CNS it is also generally believed that NE released from descending pathways can mitigate pain sensations via eliciting inhibitory effects on alpha-2A-adrenoceptors on central terminals of primary afferent nociceptors, by direct alpha-2-adrenergic action on pain-relay neurons, and by alpha-1-adrenoceptor-mediated activation of inhibitory interneurons. Such NE pain mitigation is consequently also enhanced by milnacipran's ability to enhance the presence of NE by inhibiting its reuptake via norepinephrine transporters at synaptic clefts

PW145748

Pw145748 View Pathway
drug action

Levonordefrin Drug Metabolism Action Pathway

Homo sapiens

PW126879

Pw126879 View Pathway
drug action

Levonorgestrel Action Pathway

Homo sapiens
Levonorgestrel (LNG) is a progestin (synthetic progestogen) found in contraceptives (birth control) that are taken orally, in subdermal implants or in intrauterine devices (IUD). Oral contraceptives and IUDs have a low dose, while emergency contraceptives (Plan B) are administered at high doses. This drug's contraceptive function delays or inhibits ovulation and thickens cervical mucus to prevent pregnancy before fertilization and implantation. This drug can also be used for hormone therapy in menopausal women. Levonorgestrel acts on the hypothalamic–pituitary-gonadal axis (HPG axis) where it binds to the progesterone and the androgen receptors. This binding inhibits the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH secretion is required to activate a luteinizing hormone (LH) surge that leads to ovulation. By its inhibition, the absence of LH results in no release of a viable egg from the ovaries. The thickening of the mucus interferes with sperm migration into the uterus for fertilization. An overdose of levonorgestrel may cause nausea and withdrawal bleeding.