The isomer of fucosterol, isofucosterol, has been identified as a minor constituent of marine sponge, Gynostemma pentafillum, oat seeds and a few other plants. Isofucosterol of marine sponge is believed to be the biosynthetic precursors of the antiviral orthoesterols and weinbersterols found in the same sponge. Isofucosterol exhibits lipase inhibitory effect, suggesting that it has potential as anti-obesity agent.

The mixture of artemotil and alpha-arteether is used in patients with cerebral malaria. Both beta and alpha/beta arteether have comparable activity and are curative at a dose of 5 mg/kg for 3 days against blood-induced Plasmodium cynomolgi B infection in the rhesus monkey; alpha arteether alone is slightly less active, with a 50% cure rate at the above dose. Alpha-arteether is a fourth generation anti-bacterial and anti-fungal drug. Alpha-arteether was found to inhibit the growth of E-coli strains defective in DNA-gyrase enzyme. DNA gyrase mutants were sensitive to α-arteether whereas the wild type of E-coli having intact DNA gyrase genes were not sensitive to α-arteethers. In fact, the isomer of this compound, β-arteether, does not exhibit this activity. The beta-isomer of arteether was characterized by a longer elimination half-life and a relatively larger volume of distribution than the alpha-isomer, suggesting that beta-arteether may be responsible for the prolonged in vivo schizontocidal activity.

Epoxomicin was originally isolated from the culture medium of an Actinomycetes strain based on its in vivo antitumor activity against murine B16 melanoma. Epoxomicin is a selective proteasome inhibitor with anti-inflammatory activity. Despite its promising antitumor activity, epoxomicin did not draw much attention as a potential drug lead from the pharmaceutical industry, presumably because epoxomicin has seemingly poor drug-like properties, namely the presence of a peptide backbone and the labile epoxy ketone pharmacophore. Despite its drawbacks, epoxomicin’s pharmacophore was found to provide unprecedented selectivity for the proteasome. Epoxomicin also served as a scaffold for the generation of a synthetic tetrapeptide epoxyketone with improved activity.

Allocryptopine is isoquinoline alkaloid found primarily in the plant families Fumariaceae, Papaveraceae, Berberidaceae, Ranunculaceae, Rutaceae, and Sapindaceae. It have been reported to possess strong antibacterial, anti-inflammatoty, antiparasitic, antineoplastic and anti-addictive activities. Allocryptopine inhibits human acetylcholinesterase and butyrylcholinesterase. It blocks hERG current in HEK293 cells. Allocryptopine strongly enhanced the I(peak) of the T353I channel by enhancing the plasma membrane (PM) expression of Nav1.5 and rescued defective trafficking after co-incubation with HEK293 cells that carry mutation channel 24 h. A possible preparation for the treatment of HIV-1 and HIV-2 viruses containing pharmaceutically effective amounts of allocryptopine has been patented.

Dicyclohexylamine is an inhibitor of bacterial and mammalian spermidine synthase, an inhibitor of aminopropyltransferases, promotes ornithine decarboxylase activity possibly by the inhibition of spermidine biosynthesis. A possible antifungal agent in combination with 2,4,5-triochlorophenol.

Halofantrine is a blood schizonticidal antimalarial agent with no apparent action on the sporozoite, gametocyte or hepatic stages of the infection. It is used only to treat but not to prevent malaria. Has been marketed by GlaxoSmithKline as HALFAN (halofantrine hydrochloride) in 250 mg tablets indicated for the treatment of adults who can tolerate oral medication and who have mild to moderate malaria (equal to or less than 100,000 parasites/mm3) caused by Plasmodium falciparum or Plasmodium vivax. Among side effects is cardiac arrhythmia. It belongs to the phenanthrene class of compounds that includes quinine and lumefantrine. It was reported that halofantrine binds to hematin in vitro (crystal structure of the complex) and to to plasmpesin, a haemoglobin degrading enzyme unique to the malarial parasites.

Sulfadoxine is an antimalarial agent which, together with pyrimethamine, composes an FDA-approved drug, Fansidar. Sulfadoxine acts by inhibiting dihydropteroate synthase; it crosses the blood-brain barrier and achieves 30% to 60% of the plasma concentration.

Naphthoquine is an antimalarial drug first synthesized in China in 1986 but which was not developed for clinical use until the late 1990s. This drug now is used in combination for treatment of Plasmodium Falciparum and Malaria. The use of anti-malarial drug combinations with artemisinin or with one of its derivatives is now widely recommended to overcome drug resistance in falciparum as well as vivax malaria. The fixed oral dose artemisinin-naphthoquine combination (ANQ, ARCO™) is a newer artemisinin-based combination (ACT) therapy undergoing clinical assessment.

Artemotil (also known as beta-arteether) is an antimalarial artemisinin derivative, approved for the treatment of severe cases of P. falciparum malaria. The mixture of artemotil and alpha-arteether is used in patients with cerebral malaria. Most of the artemisinin compounds including artemotil are metabolized into dihydroartemisinin, which is responsible for antimalarial activity. These compounds contain stable endoperoxide bridge. The antimalarial activity of the drug thus is dependent on the cleavage of the endoperoxide by intraparasitic heme. The cleaved endoperoxide ultimately becomes a carbon centered free radical, which then functions as an alkylating agent, reacting with both heme and parasitic proteins (but not DNA). In P. falciparum, one of the principal alkylation target is the translationally controlled tumor protein (DHA-TCTP) homolog. Some intraparasitic TCTP is situated in the membrane surrounding the heme-rich food vacuole, where heme could catalyse the formation of drug-protein (DHA-TCTP) adduct and inhibit the parasite's growth.

Artenimol (dihydroartemisinin) is a derivate of antimalarial compound artemisinin. Artenimol (dihydroartemisinin) is able to reach high concentrations within the parasitized erythrocytes. Its endoperoxide bridge is thought to be essential for its antimalarial activity, causing free-radical damage to parasite membrane systems including: • Inhibition of falciparum sarcoplasmic-endoplasmic reticulum calcium ATPase, • Interference with mitochondrial electron transport • Interference with parasite transport proteins • Disruption of parasite mitochondrial function. Dihydroartemisinin in combination with piperaquine tetraphosphate (Eurartesim, EMA-approved in 2011) is indicated for the treatment of uncomplicated Plasmodium falciparum malaria. The formulation meets WHO recommendations, which advise combination treatment for Plasmodium falciparum malaria to reduce the risk of resistance development, with artemisinin-based preparations regarded as the ‘policy standard’. However, experimental testing demonstrates that, due to its intrinsic chemical instability, dihydroartemisinin is not suitable to be used in pharmaceutical formulations. In addition, data show that the currently available dihydroartemisinin preparations fail to meet the internationally accepted stability requirements.