LDN193189 is a cell-permeable, highly potent and selective BMP pathway inhibitor. It prevents Smad1, Smad5, and Smad8 phosphorylation. It is a useful tool compound to modulate stem cell differentiation (for example, neural differentiation of human ESC/iPSC in combination with SB431542). LDN-193189 blocks the production of reactive oxygen species induced by oxidized LDL during atherogenesis in human aortic endothelial cells. It was also used in animal models to treat FOP and ectopic ossification, as well as NSCLC lung cancer.

Kifunensine is an immunoactive compound originally produced by Kitasatosporia kifunense, which displays competitive inhibition against immunosuppressive factor in tumor-bearing mice. Kifunensine has also been shown to be a potent inhibitor of the purified glycoprotein processing enzyme, mannosidase I (MAN1), specifically MAN1A1, MAN1A2, MAN1B1 and MAN1C1. Kifunensine inhibits human endoplasmic reticulum α-1,2-mannosidase I and Golgi Class I mannosidases IA, IB and IC with Ki values of 130 and 23 nM, respectively. Enzymes of this class are important factors for the biosynthesis of various types of N-linked oligosaccharide structures. Inhibition of these structures by kifunensine can interfere with cell-to-cell adhesion, targeting of lysosomal hydrolases to lysosomes, and clearance of asialoglycoproteins from the serum. Kifunensine is used to suppress Endoplasmic Reticulum-Associated Degradation (ERAD) via the inhibition of endoplasmic reticulum-associated mannosidase activity. Kifunensine has shown potential for treatment of sarcoglycanopathies and lysosomal storage disorders. Orphan designation (EU/3/11/906) was granted by the European Commission to Généthon, France, for kifunensine for the treatment of beta sarcoglycanopathy, but it was withdrawn later. Kifunensine’s use as a therapeutic is currently being researched in several conditions that benefit from its ability to inhibit mannosidase I.

Echinocandin B is a naturally occurring antibiotic, isolated from Aspergillus nidulans. It acts as an inhibitor of fungal β-1,3-glucan synthase thereby disrupting the formation of the fungal cell wall. The drug itself was not developed in the clinic, but instead, it was used in the production of other echinocandin derivatives.

Aphidicolin, a tetracyclic diterpenoid obtained from the culture filtrates of Cephalosporium aphidicola and other fungi, inhibits the growth of eukaryotic cells and of certain animal viruses (SV40, Herpes and Vaccinia viruses) by selectively inhibiting the cellular replicative DNA polymerase alpha or the viral-induced DNA polymerases. The arrest of cellular or viral growth is thus due to inhibition of cellular or viral replicative DNA synthesis without interference with mitochondrial DNA synthesis, RNA, protein and nucleic acid precursors synthesis or other major metabolic pathways. The inhibition of all sensitive eukaryotic DNA polymerases by aphidicolin is competitive with respect to dCTP. Aphidicolin has thus proved extremely useful in elucidating the functional role of DNA polymerase alpha in nuclear DNA replication, of DNA polymerase gamma in mitochondrial DNA synthesis and both DNA polymerases beta and alpha in DNA repair synthesis. An important laboratory application of aphidicolin is the synchronization of the cell cycle of eukaryotic cells both in culture and in vivo. The properties of aphidicolinhave recently aroused considerable interest for its possible exploitation in al practice. The mechanism of action of this drug suggests in fact that it may be useful for controlling excessive cell proliferation in patients with cancer, psoriasis or other dermatitis with little or no adverse effect upon non-multiplying cells.

A-TRISACCHARIDE (or Blood group A trisaccharide), a core antigen fragment in ABO blood group system. It was found to be a major urinary carbohydrate depending on diet and blood type.