Cyclobenzaprine is a centrally-acting muscle relaxant which boosts levels of norepinephrine and binds to serotonin receptors in the brain to reduce spasm. Cytochromes P-450 3A4, 1A2, and, to a lesser extent, 2D6, mediate N-demethylation, one of the oxidative pathways for cyclobenzaprine. Cyclobenzaprine relieves skeletal muscle spasm of local origin without interfering with muscle function. Drowsiness, fatigue and sedation (up to 40%) is the most common side effect of Cyclobenzaprine. It may have life-threatening interactions with monoamine oxidase (MAO) inhibitors. Postmarketing cases of serotonin syndrome have been reported during combined use of cyclobenzaprine and other drugs such as selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), tramadol, bupropion, meperidine, verapamil, or MAO inhibitors.

Minocycline is a tetracycline analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant staphylococcus infections. Minocycline has many brand names one of them is minocin, Minocin is indicated in the treatment of the following infections due to susceptible isolates of the designated bacteria: Rocky Mountain spotted fever, typhus fever and the typhus group, Q fever, rickettsialpox and tick fevers caused by rickettsiae. Respiratory tract infections caused by Mycoplasma pneumoniae. Lymphogranuloma venereum caused by Chlamydia trachomatis. Psittacosis (Ornithosis) due to Chlamydophila psittaci etc. Minocycline is indicated for the treatment of infections caused by the following Gram-negative bacteria when bacteriologic testing indicates appropriate susceptibility to the drug: Escherichia coli. Enterobacter aerogenes. Shigella species etc. MINOCIN also is indicated for the treatment of infections caused by the following Gram-positive bacteria when bacteriologic testing indicates appropriate susceptibility to the drug: Upper respiratory tract infections caused by Streptococcus pneumoniae. Skin and skin structure infections caused by Staphylococcus aureus (Note: Minocycline is not the drug of choice in the treatment of any type of staphylococcal infection, etc. When penicillin is contraindicated, minocycline is an alternative drug in the treatment of the following infections: Meningitis due to Neisseria meningitidis. Syphilis caused by Treponema pallidum subspecies pallidum. Yaws caused by Treponema pallidum subspecies pertenue, etc. Minocycline passes directly through the lipid bilayer or passively diffuses through porin channels in the bacterial membrane. Minocycline inhibits protein synthesis by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.

Griseofulvin is a mycotoxic metabolic product of Penicillium spp. It was the first available oral agent for the treatment of dermatophytoses and has now been used for more than forty years. Griseofulvin is fungistatic with in vitro activity against various species of Microsporum Epidermophyton, and Trichophyton. It has no effect on bacteria or on other genera of fungi. Following oral administration, griseofulvin is deposited in the keratin precursor cells and has a greater affinity for diseased tissue. The drug is tightly bound to the new keratin which becomes highly resistant to fungal invasions. Once the keratin-Griseofulvin complex reaches the skin site of action, it binds to fungal microtubules (tubulin) thus altering fungal mitosis. Griseofulvin is fungistatic, however the exact mechanism by which it inhibits the growth of dermatophytes is not clear. It is thought to inhibit fungal cell mitosis and nuclear acid synthesis. It also binds to and interferes with the function of spindle and cytoplasmic microtubules by binding to alpha and beta tubulin. It binds to keratin in human cells, then once it reaches the fungal site of action, it binds to fungal microtubes thus altering the fungal process of mitosis.

Digoxin, a cardiac glycoside similar to digitoxin, is used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation. Digoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium. The sodium calcium exchanger (NCX) in turn tries to extrude the sodium and in so doing, pumps in more calcium. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Digoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.

Chlorpromazine is a psychotropic agent indicated for the treatment of schizophrenia. It also exerts sedative and antiemetic activity. Chlorpromazine has actions at all levels of the central nervous system-primarily at subcortical levels-as well as on multiple organ systems. Chlorpromazine has strong antiadrenergic and weaker peripheral anticholinergic activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic and antiserotonin activity. Chlorpromazine acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects). Additionally, Chlorpromazine is a weak presynaptic inhibitor of Dopamine reuptake, which may lead to (mild) antidepressive and antiparkinsonian effects. Chlorpromazine has being marketed under the trade names Thorazine and Largactil among others. Chlorpromazine is used for treating certain mental or mood disorders (eg, schizophrenia), the manic phase of manic-depressive disorder, anxiety and restlessness before surgery, the blood disease porphyria, severe behavioral and conduct disorders in children, nausea and vomiting, and severe hiccups.

Proguanil is a prophylactic antimalarial drug, which works by stopping the malaria parasite, Plasmodium falciparum and Plasmodium vivax, from reproducing once it is in the red blood cells. Proguanil in combination with atovaquone are marked under the brand name malarone, which is indicated for the treatment of acute, uncomplicated P. falciparum malaria and for the prophylaxis of Plasmodium falciparum malaria, including in areas where chloroquine resistance has been reported. Atovaquone and proguanil, interfere with 2 different pathways involved in the biosynthesis of pyrimidines required for nucleic acid replication. Atovaquone is a selective inhibitor of parasite mitochondrial electron transport. Proguanil hydrochloride primarily exerts its effect by means of the metabolite cycloguanil, a dihydrofolate reductase inhibitor. Inhibition of dihydrofolate reductase in the malaria parasite disrupts deoxythymidylate synthesis. Recently were done experiments, which confirmed the hypothesis that proguanil might act on another target than dihydrofolate reductase. In addition, was made conclusion, that effectiveness of malarone was due to the synergism between atovaquone and proguanil and may not require the presence of cycloguanil.

Oxytetracycline, a tetracycline analog isolated from the actinomycete streptomyces rimosus, was the second of the broad-spectrum tetracycline group of antibiotics to be discovered The drug is used for the prophylaxis and local treatment of superficial ocular infections due to oxytetracycline- and polymyxin-sensitive organisms for animal use only. These infections include the following: Ocular infections due to streptococci, rickettsiae E. coli, and A. aerogenes (such as conjunctivitis, keratitis, pinkeye, corneal ulcer, and blepharitis in dogs); ocular infections due to secondary bacterial complications associated with distemper in dogs; and ocular infections due to bacterial inflammatory conditions which may occur secondary to other diseases in dogs. Allergic reactions may occasionally occur. Treatment should be discontinued if reactions are severe. If new infections due to nonsensitive bacteria or fungi appear during therapy, appropriate measures should be taken. Oxytetracycline inhibits cell growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. The binding is reversible in nature. Oxytetracycline is lipophilic and can easily pass through the cell membrane or passively diffuses through porin channels in the bacterial membrane.

Dideoxyadenosine (2′,3′-dideoxyadenosine) is a prodrug form of didanosine (2',3'-dideoxyinosine), a nucleoside reverse transcriptase inhibitor analog of adenosine. 2',3'-Dideoxyadenosine and 2',3'-dideoxyinosine were shown to be equally effective in the inhibition of HIV proliferation in human T cells. Dideoxyadenosine competitively inhibits adenylyl cyclase, thereby reducing levels of cyclic adenosine monophosphate (cAMP). By inhibiting cAMP-mediated gene activation in tumor cells, this agent may retard tumor cell proliferation. 2',3'-dideoxyadenosine inhibits retroviral DNA synthesis and mRNA expression in T cells exposed to the virus that causes acquired immunodeficiency syndrome, and affords such cells long-term protection in vitro under conditions of substantial viral excess. 2',3'-dideoxyadenosine appears to completely block reverse transcription from viral RNA to viral DNA. 2',3'-dideoxyadenosine was also shown not only to possess antibacterial activity in vitro against a variety of Enterobacteriaceae, but also to be effective in vivo, dideoxyadenosine was active in experimental mouse infections by the oral route against 5 Salmonella strains, 2 of 3 Arizona strains, 5 of 7 Citrobacter strains, 3 of 8 Klebsiella strains, 3 of 5 Escherichia strains, 1 of 3 Shigella strains, and 3 of 15 Serratia strains at concentrations generally well below the toxic level.

11-Deoxycortisol (also known as cortodoxone) is the predominant deoxycorticosteroid and is the immediate precursor of cortisol, which is formed by the enzymatic action of 11beta-hydrozylase (P450). Deficiency of this enzyme causes congenital adrenal hyperplasia, which is characterized by hypertension. 11-deoxycortisol is measured as part of the Metyrapone Test. Metyrapone blocks the formation of cortisol, resulting in increased secretion of Adrenocorticotropic hormone (ACTH) and 11-deoxycortisol in normal individuals.