Dihydromorphine is a semi-synthetic opioid derived from morphine. dihydromorphine is a moderately strong analgesic and is used clinically in the treatment of pain and is also the active metabolite of dihydrocodeine. Dihydromorphine acts as an agonist at the μ-opioid (mu), δ-opioid (delta) and κ-opioid (kappa) receptors. Dihydromorphone is approved for clinical use in the United States, Europe, and Japan; and sold under the brand name Dilaudid. Similar to morphine, and other morphine derivatives, hydromorphone has a high potential for addiction and abuse and is listed as a Schedule II drug in the United States Controlled Substances Act of 1970 (and similarly regulated in other countries).

Esatenolol is the (S) enantiomer of atenolol, a beta1-adrenergic receptor antagonist. Only (S)-atenolol, but not (R)-atenolol, contributes to the beta-blocking effect of currently used racemic atenolol since the same effect can be elicited with the (S)-enantiomer alone. Pure (S)-atenolol has been launched in India for the treatment of hypertension and angina pectoris.

Timolol is the non-selective Beta antagonist used as eye drops to treat increased pressure inside the eye such as in ocular hypertension and glaucoma. Timolol is also used for high blood pressure, chest pain due to insufficient blood flow to the heart, to prevent further complications after a heart attack, and to prevent migraines. Timolol is a beta1 and beta2 (non-selective) adrenergic receptor antagonist that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anesthetic (membrane-stabilizing) activity. Timolol, when applied topically on the eye, has the action of reducing elevated, as well as normal intraocular pressure, whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss and optic nerve damage. The precise mechanism of the ocular hypotensive action of Timolol is not clearly established at this time. Tonography and fluorophotometry studies of the timolol maleate ophthalmic solution in man suggest that its predominant action may be related to the reduced aqueous formation. However, in some studies, a slight increase in outflow facility was also observed. In a study of plasma drug concentration in six subjects, the systemic exposure to timolol was determined following once daily administration of Timolol Maleate Ophthalmic Gel Forming Solution 0.5% in the morning. The mean peak plasma concentration following this morning dose was 0.28 ng/mL. Side effects, when given in the eye, include burning sensation, eye redness, superficial punctate keratopathy, corneal numbness.

Timolol is the non-selective Beta antagonist used as eye drops to treat increased pressure inside the eye such as in ocular hypertension and glaucoma. Timolol is also used for high blood pressure, chest pain due to insufficient blood flow to the heart, to prevent further complications after a heart attack, and to prevent migraines. Timolol is a beta1 and beta2 (non-selective) adrenergic receptor antagonist that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anesthetic (membrane-stabilizing) activity. Timolol, when applied topically on the eye, has the action of reducing elevated, as well as normal intraocular pressure, whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss and optic nerve damage. The precise mechanism of the ocular hypotensive action of Timolol is not clearly established at this time. Tonography and fluorophotometry studies of the timolol maleate ophthalmic solution in man suggest that its predominant action may be related to the reduced aqueous formation. However, in some studies, a slight increase in outflow facility was also observed. In a study of plasma drug concentration in six subjects, the systemic exposure to timolol was determined following once daily administration of Timolol Maleate Ophthalmic Gel Forming Solution 0.5% in the morning. The mean peak plasma concentration following this morning dose was 0.28 ng/mL. Side effects, when given in the eye, include burning sensation, eye redness, superficial punctate keratopathy, corneal numbness.

Hydromorphone (also known as dihydromorphinone and the brand name Dilaudid among others) is a more potent opioid analgesic than morphine and is used for moderate to severe pain. It can be administered by injection, by infusion, by mouth, and rectally. Oral bioavailability is low. The kidney excretes hydromorphone and its metabolites. Some metabolites may have greater analgesic activity than hydromorphone itself but are unlikely to contribute to the pharmacological activity of hydromorphone. With the exception of pruritus, sedation and nausea and vomiting, which may occur less after hydromorphone than after morphine, the side-effects of these drugs are similar. Hydromorphone interacts predominantly with the opioid mu-receptors. These mu-binding sites are discretely distributed in the human brain, with high densities in the posterior amygdala, hypothalamus, thalamus, nucleus caudatus, putamen, and certain cortical areas. It also binds with kappa and delta receptors which are thought to mediate spinal analgesia, miosis and sedation.

Hydromorphone (also known as dihydromorphinone and the brand name Dilaudid among others) is a more potent opioid analgesic than morphine and is used for moderate to severe pain. It can be administered by injection, by infusion, by mouth, and rectally. Oral bioavailability is low. The kidney excretes hydromorphone and its metabolites. Some metabolites may have greater analgesic activity than hydromorphone itself but are unlikely to contribute to the pharmacological activity of hydromorphone. With the exception of pruritus, sedation and nausea and vomiting, which may occur less after hydromorphone than after morphine, the side-effects of these drugs are similar. Hydromorphone interacts predominantly with the opioid mu-receptors. These mu-binding sites are discretely distributed in the human brain, with high densities in the posterior amygdala, hypothalamus, thalamus, nucleus caudatus, putamen, and certain cortical areas. It also binds with kappa and delta receptors which are thought to mediate spinal analgesia, miosis and sedation.

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.

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.

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.

Valproic acid (VPA; valproate; di-n-propylacetic acid, DPA; 2-propylpentanoic acid, or 2-propylvaleric acid) was first synthesized in 1882, by Burton. FDA approved valproic acid for the treatment of manic episodes associated with bipolar disorder, for the monotherapy and adjunctive therapy of complex partial seizures and simple and complex absence seizures and adjunctive therapy in patients with multiple seizure types that include absence seizures and for the prophylaxis of migraine headaches. The mechanisms of VPA which seem to be of clinical importance in the treatment of epilepsy include increased gamma-aminobutyric acid (GABA)-ergic activity, reduction in excitatory neurotransmission, and modification of monoamines. Recently, it was discovered that the VPA is a class I selective histone deacetylase inhibitor. This activity can be distinguished from its therapeutically exploited antiepileptic activity.