Pentazocine is a synthetically prepared prototypical mixed agonist-antagonist narcotic (opioid analgesic) drug of the benzomorphan class of opioids used to treat moderate to moderately severe pain. Pentazocine is sold under several brand names, such as Fortral, Sosegon, Talwin NX. Pentazocine acts as an agonist of κ-opioid receptors and as an antagonist of μ-opioid receptors. This compound may exist as one of two enantiomers, named (+)-pentazocine and (−)-pentazocine. Side effects are similar to those of morphine, but pentazocine, due to its action at the kappa opioid receptor is more likely to invoke psychotomimetic effects. High dose may cause high blood pressure or high heart rate.

Nalbuphine is a semi-synthetic opioid agonist-antagonist used commercially as an analgesic under a variety of trade names, including Nubain and Manfine. Nalbuphine is an agonist at kappa opioid receptors and an antagonist at mu opioid receptors. Nalbuphine analgesic potency is essentially equivalent to that of morphine on a milligram basis up to a dosage of approximately 30 mg. The opioid antagonist activity of Nalbuphine is one-fourth as potent as nalorphine and 10 times that of pentazocine. Nalbuphine is indicated for the management of pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Nalbuphine can also be used as a supplement to balanced anesthesia, for preoperative and postoperative analgesia, and for obstetrical analgesia during labor and delivery. The onset of action of Nalbuphine occurs within 2 to 3 minutes after intravenous administration, and in less than 15 minutes following subcutaneous or intramuscular injection. The plasma half-life of nalbuphine is 5 hours, and in clinical studies, the duration of analgesic activity has been reported to range from 3 to 6 hours. Like pure µ-opioids, the mixed agonist-antagonist opioid class of drugs can cause side effects with initial administration of the drug but which lessen over time (“tolerance”). This is particularly true for the side effects of nausea, sedation and cognitive symptoms. These side effects can in many instances be ameliorated or avoided at the time of drug initiation by titrating the drug from a tolerable starting dose up to the desired therapeutic dose. An important difference between nalbuphine and the pure mu-opioid analgesic drugs is the “ceiling effect” on respiration. Respiratory depression is a potentially fatal side effect from the use of pure mu opioids. Nalbuphine has limited ability to depress respiratory function.

Vincristine is a vinca alkaloid antineoplastic agent used as a treatment for various cancers including breast cancer, Hodgkin's disease, Kaposi's sarcoma, and testicular cancer. The vinca alkaloids are structurally similar compounds comprised of 2 multiringed units, vindoline and catharanthine. The vinca alkaloids have become clinically useful since the discovery of their antitumour properties in 1959. Initially, extracts of the periwinkle plant (Catharanthus roseus) were investigated because of putative hypoglycemic properties, but were noted to cause marrow suppression in rats and antileukemic effects in vitro. Vincristine binds to the microtubular proteins of the mitotic spindle, leading to crystallization of the microtubule and mitotic arrest or cell death. Vincristine has some immunosuppressant effect. The vinca alkaloids are considered to be cell cycle phase-specific. The antitumor activity of Vincristine is thought to be due primarily to inhibition of mitosis at metaphase through its interaction with tubulin. Like other vinca alkaloids, Vincristine may also interfere with: 1) amino acid, cyclic AMP, and glutathione metabolism, 2) calmodulin-dependent Ca2+-transport ATPase activity, 3) cellular respiration, and 4) nucleic acid and lipid biosynthesis.Vincristine was marketed under the brand name Oncovin, but was discontinued. In 2012 the FDA approved a Liposomal formulation of Vincristine, named MARQIBO KIT.

Vinblastine is a Vinca alkaloid obtained from the Madagascar periwinkle plant. Vinca alkaloids were found out in the 1950's by Canadian scientists, Robert Noble and Charles Beer for the first time. Medicinal applications of this plant lead to the monitoring of these compounds for their hypoglycemic activity, which is of little importance compared to their cytotoxic effects. They have been used to treat diabetes, high blood pressure and the drugs have even been used as disinfectants. Nevertheless, the vinca alkaloids are so important for being cancer fighters. The mechanism of action of vinblastine sulfate has been related to the inhibition of microtubule formation in the mitotic spindle, resulting in an arrest of dividing cells at the metaphase stage. Vinblastine is an antineoplastic agent used to treat Hodgkin's disease, non-Hodgkin's lymphomas, mycosis fungoides, cancer of the testis, Kaposi's sarcoma, Letterer-Siwe disease, as well as other cancers.

Oxymorphone is an analgesic that is FDA approved for the treatment of moderate to severe pain. It is also indicated for relief of anxiety in patients with dyspnea associated with pulmonary edema secondary to acute left ventricular dysfunction. Oxymorphone (brand names Opana, Numorphan, Numorphone) is a full opioid agonist and is relatively selective for the mu-opioid receptor, although it can bind to other opioid receptors at higher doses. Adverse reactions (≥ 2% of patients): seen with the immediate release tablet formulation Nausea, pyrexia, somnolence, vomiting, pruritus, headache, dizziness, constipation, and confusion. Concomitant use with serotonergic drugs may result in serotonin syndrome. Avoid use of mixed agonist/antagonist and partial agonist opioid analgesics with Opana because they may reduce analgesic effect of Opana or precipitate withdrawal symptoms.

Levorphanol, brand name Levo-Dromoran, is an opioid medication used to treat moderate to severe pain. Levorphanol is indicated for the management of moderate to severe pain where an opioid analgesic is appropriate. It is a potent synthetic opioid mu-receptor agonist similar in action to morphine. Like other opioid mu-receptor agonists, it is believed to act at receptors in both the brain and spinal cord to alter the transmission and perception of pain. The onset and peak analgesic effects following administration of levorphanol are similar to morphine when administered at equal analgesic doses. Levorphanol produces a degree of respiratory depression similar to that produced by morphine at equal analgesic doses, and like many opioid mu-receptor agonists, levorphanol produces euphoria or has a positive effect on mood in many individuals.

Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).

Methadone, sold under the brand names Dolophine among others, is an synthetic opioid that is used as the hydrochloride to treat pain and as maintenance therapy or to help with detoxification in people with opioid dependence. Methadone hydrochloride is a mu-agonist; a synthetic opioid analgesic with multiple actions qualitatively similar to those of morphine. Some data also indicate that methadone acts as an antagonist at the NMDA-receptor. The contribution of NMDA receptor antagonism to methadone’s efficacy is unknown. Most common adverse reactions are: lightheadedness, dizziness, sedation, nausea, vomiting, and sweating. Avoid use mixed agonist/antagonist and partial agonist opioid analgesics with DOLOPHINE because they may reduce analgesic effect of DOLOPHINE or precipitate withdrawal symptoms.

Benzhydrocodone is a prodrug of hydrocodone. Benzhydrocodone is formed by covalently bonding hydrocodone to benzoic acid. Benzhydrocodone itself is not pharmacologically active, but must be metabolized to hydrocodone by enzymes in the intestinal tract to optimally deliver its pharmacologic effects. Hydrocodone is a full agonist of the opioid receptors with a higher affinity for the mu-opioid receptor. Upon binding, hydrocodone produces an analgesic effect with no ceiling. APADAZ a combination of benzhydrocodone and acetaminophen is FDA approved and indicated for the short-term (no more than 14 days) management of acute pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. APADAZ, even when taken as recommended, can result in addiction, abuse, and misuse, which can lead to overdose and death.

Since its discovery as component of the tea leaf by Albert Kossel in 1888, the history of theophylline (CAS 58-55-9) has been a long and successful one. At the turn of the century, theophylline became less expensive due to chemical synthesis and was primarily used as diuretic in subsequent years. It was Samuel Hirsch who discovered the bronchospasmolytic effect of theophylline in 1992, however, despite this pioneering discovery theophylline continued to be used primarily as diuretic and cardiac remedy. The molecular mechanism of bronchodilatation is inhibition of phosphodiesterase(PDE)3 and PDE4, but the anti-inflammatory effect may be due to histone deacetylase (HDAC) activation, resulting in switching off of activated inflammatory genes. Theophylline is indicated for the treatment of acute exacerbations of the symptoms and reversible airflow obstruction associated with asthma and other chronic lung diseases, e.g., emphysema and chronic bronchitis.