Pathways

Naltrexone (also known as ReVia and Vivitrol) is a competitive antagonist of mu-type opioid receptor in the central nervous system (CNS). Naltrexone is also a type of medication that are used for manage opioid or alcohol dependence. Binding of naltrexone can prevent the effects that caused by endogenous opioids, which results in antagonization of effects of opiates such as respiratory depression or drug craving.

Naltrexone is a narcotic antagonist used in opioid overdose. It is injected intravenously or intramuscularly. It travels through the blood to the target cells in the naltrexone pathway and to the liver. It is transported into the liver by an organic cation transporter. In the liver naltrexone is metabolized into 6-beta-naltrexol. It was predicted by biotransformer that Cytochrome P450 2C9 metabolizes naltrexone into 6-beta-naltrexol. However, it has also been found that Naltrexone in certain doses inhibits cytochrome enzymes. Only 2% of naltrexone remains as the original naltrexone while the remainder is metabolized into 6-beta-naltrexol and other minor metabolites. Naltrexone and 6-beta-naltrexol are transported out of the liver by organic cation transporters into the blood. It is then transported to the kidney where it is excreted renally. 53% to 79% of the dose is excreted as metabolites. A minor amount goes through bile to be excreted through the feces.

Naltrexone is a narcotic antagonist used in opioid overdose.. It is also used to treat alcohol dependence in conjunction with behavioural programs. Naltrexone inhibits Mu, Kappa, and Delta opioid receptors, with the highest affinity for the mu-type opioid receptors. This inhibits the exchange of GTP for GDP which is required to activate the G-protein complex. This prevents the Gi subunit of the mu opioid receptor from inhibiting adenylate cyclase, which can therefore continue to catalyze ATP into cAMP. cAMP increases the excitability in spinal cord pain transmission neurons which allows the patient to feel pain rather than the analgesic effects of opioids. The inhibition of Mu-type opioid receptors also prevents the Gi subunit of the mu opioid receptor from activating the inwardly rectifying potassium channel increasing K+ conductance which would cause hyperpolarization. Naltrexone also prevents the gamma subunit of the mu opioid receptor from inhibiting the N-type calcium channels on the neuron. This allows calcium to enter the neuron and depolarize. The inhibition of mu-opioid receptors prevents hyperpolarization in the neuron, allowing it to fire at a normal rate. The neuron is able to depolarize and the high concentration of calcium releases GABA into the synapse which binds to GABA receptors. GABA receptors inhibits dopamine cell firing in the pain transmission neurons. This prevents the analgesic and depressive effects of opioids, preventing opioid overdose. GABA also inhibits dopamine cell firing in the reward pathway which is the main cause of addiction to opioids and other drugs. The major metabolite, 6-β-naltrexol is also a opioid antagonist that may contribute to the effects of naltrexone.

Metabolites of Naphazoline are predicted with biotransformer.

Naphthalene degradation involves a series of enzymatic reactionsin which bacteria use as both a carbon and energy source. Naphthalene, a polycyclic aromatic hydrocarbon (PAH), enters bacterial cells by passive diffusion across the cell membrane due to its hydrophobicity. Once within the cell, naphthalene is activated by the enzyme naphthalene dioxygenase, which produces cis-1,2-dihydroxynaphthalene. This intermediate is further metabolized by a series of enzymatic reactions, including ring cleavage, hydroxylation, and oxidation, to produce metabolites such as Gentisate and Catechol, which enter the Tyrosine metabolism and benzoate degradation pathways for energy generation and biosynthesis.

Naproxen (also named Aleve and Naprosyn) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to relieve pain (analgesic) and reduce fever (antipyretic). Naproxen is also a type of ophthalmic anti-inflammatory medicines. Naproxen can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Since prostaglandin is the messenger molecules in the process of inflammation; hence, inhibition of prostaglandin synthesis can reduce the pain and inflammation.