Pantoprazole is a proton pump inhibitor that inhibits gastric acid secretion and used for short-term treatment of erosive esophagitis associated with gastroesophageal reflux disease. Pantoprazole suppresses the final step in gastric acid production by covalently binding to the (H+, K+)-ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. The binding to the (H+, K+)-ATPase results in a duration of antisecretory effect that persists longer than 24 hours. Pantoprazole is used for short-term treatment of erosion and ulceration of the esophagus for adults and pediatric patients 5 years of age and older caused by gastroesophageal reflux disease. It can be used as a maintenance therapy for long-term use after initial response is obtained, but there have not been any controlled studies about the use of pantoprazole past a duration of 12 months. Pantoprazole may also be used in combination with antibiotics to treat ulcers caused by Helicobacter pylori. Use of pantoprazole may increase the chance of developing infections such as pneumonia, particularly in hospitalized patients.

Adrogolide is a chemically stable prodrug of the dopamine D1 receptor agonist A-86929. Adrogolide is rapidly converted in plasma to A-86929. A-86929 has high affinity and functional selectivity for the dopamine D1 receptor. Adrogolide has been in phase II clinical trials for the treatment of Parkinson's disease and cocaine abuse. However, this research has been discontinued. The adverse events associated with its use of adrogolide were of mild-to-moderate severity and included injection site reaction, asthenia, headache, nausea, vomiting, postural hypotension, vasodilitation, and dizziness.

Withaferin A is one of the most bioactive phytoconstituents of Withania somnifera, a well-known herb in Ayurvedic medical tradition of India. Due to the lactonal steroid's potential to modulate multiple oncogenic pathways, Withaferin A has gained much attention as a possible anti-neoplastic agent. Systematic research on the evaluation of anticancer activities of withaferin A was started around the 1970s. Since then, a large number of studies have demonstrated the ability of withaferin A to suppress the in vivo growth of various human cancer cells’ xenograft tumors as well as experimentally induced carcinogenesis in different rodent models. It has being reported that withaferin-A reduced the growth of human prostate cancer (PC3) cells tumor xenograft in nude mice by blocking the tumor angiogenesis and inducing intratumoral apoptosis. According to this study, i.p. administration of withaferin-A caused regression of implanted tumor cells by decreasing the expression of angiogenesis marker CD31, inducing the expression of proapoptotic protein Bax, and activating caspase-3 via inhibition of nuclear factor-κB (NF-κB) signaling pathway. In a separate study, intratumoral administration of withaferin-A arrested PC3 cells’ xenograft tumor growth in mice by inducing tumor cell death via upregulation of prostate apoptosis response-4 (Par-4). Anticancer activity of withaferin-A has also being demonstrated for gynecological cancer, melanoma, thyroid, gastrointestinal and other types of cancer. Mechanistic basis of the anticancer effects of withaferin-A includes: (1) reinforcement of cellular antioxidant and/or detoxification system; (2) suppression of inflammatory pathways; (3) selective inhibition of tumor cell proliferation and induction of apoptosis; (4) suppression of tumor angiogenesis; (5) blockade of epithelial-to-mesenchymal transition (EMT), tumor invasion, and metastasis; (6) alteration of tumor cell metabolism; (7) immunomodulation; and (8) eradication of cancer stem cells.

Calanolide A is a new non-nucleoside reverse transcriptase inhibitor (NNRTI) originally extracted from a tropical tree (Calophyllum lanigerum) in the Malaysian rain forest. Viral life-cycle studies indicate that calanolide A acts early in the infection process, similar to the known HIV reverse transcriptase (RT) inhibitor 2', 3'-dideoxycytidine. In enzyme inhibition assays, calanolide A potently and selectively inhibits recombinant HIV type 1 RT but not cellular DNA polymerases or HIV type 2 RT within the concentration range tested. Phase I studies have found that calanolide A is well tolerated. Consequently, it has potential clinical applications in combination with other antiviral drugs to suppress HIV-1 mutants. Nevertheless, the development of calanolide A has been delayed due to its low therapeutic index (range: 16–279), non-ideal antiviral activity, and the complexity of its extraction from plants