Pathways

Nafcillin is a penicillin derivative antibiotic used to treat susceptible staphylococcal and streptococcal infections. Like other penicillins, nafcillin exerts a bactericidal action against penicillin-susceptible microorganisms during the state of active multiplication in the bacterial cell wall synthesis. It inhibits the biosynthesis of the bacterial cell wall by forming covalent bonds with penicillin-binding proteins that play a critical role in the final transpeptidation process. Binding to penicillin-binding proteins inhibits the transpeptidase and carboxypeptidase activities conferred by these proteins and prevents the formation of the crosslinks.

Naftifine is an antifungal agent used to treat infections of the Tinea, Trichophyton, and Epidermophyton species. It is used as a topical treatment of tinea pedis, tinea cruris, and tinea corporis caused by the organisms Trichophyton rubrum, Trichophyton mentagrophytes, Trichophyton tonsurans and Epidermophyton floccosum. Naftifine is a synthetic, broad spectrum, antifungal agent and allylamine derivative. Naftifine has been shown to exhibit fungicidal activity in vitro against a broad spectrum of organisms including Trichophyton rubrum, Trichophyton mentagrophytes, Trichophyton tonsurans, Epidermophyton floccosum, and Microsporum canis, Microsporum audouini, and Microsporum gypseum; and fungistatic activity against Candida species including Candida albicans. However it is only used to treat the organisms listed in the indications. Although the exact mechanism of action against fungi is not known, naftifine appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2,3-epoxidase, also known as, squalene monooxygenase. Squalene monooxygenase catalyzes the synthesis of (S)-2,3-epoxysqualene from squalene. Since it is inhibited, it cannot continue on to synthesize lanosterol which is essential in the synthesis of ergosterol. Without ergosterol in the cell membrane, the cell membrane sees increased permeability which allows intracellular components to leak out of the cell. Ergosterol is also essential in cell membrane integrity so without that, eventually the cell collapses and dies.. The fungal cell also cannot synthesize new cell membranes for new fungus cells if there is no ergosterol. The inhibition of squalene monooxygenase also causes a buildup of squalene which is toxic to the fungal cell.

Nalbuphine (also known as Rubuphine and Nubain) is a competitive antagonist of mu-type and kappa-type opioid receptor in the central nervous system (CNS). Nalbuphine is also a type of medication that are mainly used for treat pain. Binding of nalbuphine can prevent the effects that caused by endogenous opioids, which results in antagonization of effects of opiates such as respiratory depression or drug craving.

Nalbuphine, also known as Rubuphine and Nubain, is a synthetic opioid agonist-antagonist. This drug is thus an analgesic used to treat pain, for pre and postoperative analgesia, and for analgesia in labor and delivery (moderate to severe pain). This narcotic is an agonist to kappa-opioid receptors and an antagonist or partial agonist at mu-opioid receptors in the central nervous system (CNS) (probably in or associated with the limbic system). The binding of nalbuphine can prevent the effects caused by endogenous opioids, which antagonizes the impact of opiates such as respiratory depression or drug craving. Nalbuphine's analgesic potency is equivalent to morphine on a milligram basis. Symptoms of overdose include primarily sleepiness and mild dysphoria. Nalbuphine is administered as an intramuscular/intravenous/subcutaneous injections. Nalbuphine 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. Nalbuphine 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.