Ditercalinium is the antineoplastic agent. Ditercalinium itself is not a natural product, however, it is derived from the natural product 5,11-dimethyl-6H-pyrido-[4,3- b]carbazole (ellipticine) that was isolated in 1959. It is a rare example of a noncovalent DNA-binding ligand that forms bisintercalation complexes via the major groove of the double helix. Ditercalinium selectively recognizes certain GC-rich sequences in DNA. It preferentialy binds with antiparallel quadruplex sequence d(AG(3)[T(2)AG(3)](3)). Ditercalinium chloride can deplete mitochondrial DNA in both mouse and human cells. Ditercalinium chloride inhibits human DNA polymerase gamma activity as efficiently as does ethidium bromide. Ethidium bromide distributes diffusely in the mitochondria of HeLa cells, while ditercalinium chloride distributes granularly and hence may be strongly associated with mitochondrial DNA.

Pretamazium is thiazolium derivative patented by UK pharmaceutical company Wellcome Foundation Ltd. as antiphrastic compound, that active against parasitic nematodes.

Butoxylate is organic compound with significant analgesic or mydriatic activity after s.c. injection in mice and rats

Butopiprine is alkoxyethyl α-phenyl-α-piperidinoacetate possessing spasmolytic, local anesthetic, and antitussive activity.

Butocrolol amino alcohol derivative with β-adrenolytic, antiarrhythmic, and local anesthetic properties having sympatholytic and antiarrhythmic effects comparable to those of propranolol, but with lower local anesthetic effects.

Doreptide is the most active analog of PLG (Pro-Leu-Gly-NH2). It was evaluated as L-dopa potentiating agent for the treatment of Parkinson's disease.

Doxaminol is a recently developed beta-sympathomimetic agent, which has shown promising positive inotropic activity in experimental animal models. It is a dibenzoxepine derivative. In normal volunteers, doxaminol exhibits effects on noninvasive cardiological indices similar to those observed after cardiac glycosides. After single-dose application of doxaminol in cases of congestive heart failure, cardiac output and stroke volume increased, heart rate increased slightly, pulmonary and systemic arterial pressure remained constant, and peripheral vascular resistance decreased. No arrhythmias appeared, but one patient suffered an attack of angina.

Amustaline (S-303) is a quinacrine mustard compound with potential antineoplastic activity. Amustaline binds to, intercalates and crosslinks DNA and RNA. This agent is mainly used for ex vivo purposes, specifically for the inactivation of pathogens such as viruses, protozoa and bacteria in red blood cells (RBCs). When S-303 is added to red blood cells, the compound rapidly passes through membranes, including those of cells and viral envelopes, due to its amphipathic character, and intercalates into helical regions of the nucleic acids of pathogens and white blood cells. TERCEPTTMBlood System usingamustaline (S-303) and glutathione (GSH) was able to inactivate high levels of DENV and ZIKV in RBCs. S-303 system has been shown to effectively inactivate a broad spectrum of pathogens, while maintaining RBC quality.

Amotosalen (S-59, psoralen derivative), a chemical capable of binding to nucleic acids is added to platelets. UVA illumination (320 – 400 nm wavelengths) of amotosalen-treated platelet components induces covalent cross-linking of any nucleic acids to which amotosalen is bound; thereby, preventing further replication. Amotosalen is used in the INTERCEPT process to cross-link DNA and RNA. Amotosalen has protective activity against pathogens such as bacteria, viruses, protozoa, and leukocytes. Prior to administration amotosalen is added to plasma and platelets, then in vivo this agent penetrates pathogens and targets DNA and RNA. Upon activation by ultraviolet A light, amotosalen forms interstrand DNA and RNA crosslinks and prevents replication. Thus, the pathogen-inactivation system using amotosalen/ultraviolet A offers the potential to mitigate the risk of ZIKV transmission by plasma and platelet transfusion. Inactivation of leukocytes can prevent graft versus host disease upon transfusion.