23282-20-4
Chemical Structure
Nivalenol
- CAS No.: 23282-20-4
- Formula:C15H20O7
- Molecular Weight:312.32
IUPAC Name: (2'R,3'R,4'S,5a'R,6'S,9a'R)-3',4',6'-trihydroxy-5a'-(hydroxymethyl)-5',8'-dimethyl-2',3',4',5',5a',9a'-hexahydrospiro[oxirane-2,10'-[2,5]methanobenzo[b]oxepin]-7'(6'H)-one
InChIKey: UKOTXHQERFPCBU-NVRDWZTOSA-N
SMILES: CC12C3(CO3)[C@@](O[C@@]4([H])[C@]2(CO)[C@@H](C(C(C)=C4)=O)O)([H])[C@H](O)[C@H]1O
Biological Activity: Nivalenol, a trichothecene mycotoxin that can be produced by Fusarium graminearum, is a fungal metabolite present in agricultural product. Nivalenol modulates apoptotic pathway, cell cycle regulation, Bax, ERK, caspase-3, and poly-ADP-ribose synthase activity in macrophages. Nivalenol inhibits ribosomal peptidyltransferase site, protein synthesis, DNA synthesis, and cell proliferation. Nivalenol induces late-stage apoptotic morphological changes, reduces cellular metabolism, and decreases cell proliferation in erythroleukemia cells. Nivalenol induces lymphocyte apoptosis in murine thymus, spleen, and Peyer's patches. Nivalenol can be used for the research of erythroleukemia[1][2][3].
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Nivalenol | 99.9% | Nivalenol, a trichothecene mycotoxin that can be produced by Fusarium graminearum, is a fungal metabolite present in agricultural product. Nivalenol modulates apoptotic pathway, cell cycle regulation, Bax, ERK, caspase-3, and poly-ADP-ribose synthase activity in macrophages. Nivalenol inhibits ribosomal peptidyltransferase site, protein synthesis, DNA synthesis, and cell proliferation. Nivalenol induces late-stage apoptotic morphological changes, reduces cellular metabolism, and decreases cell proliferation in erythroleukemia cells. Nivalenol induces lymphocyte apoptosis in murine thymus, spleen, and Peyer's patches. Nivalenol can be used for the research of erythroleukemia. | ||||||||||||||||||||
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Nivalenol (Standard) | ≥98% | Nivalenol (Standard) is the analytical standard of Nivalenol (HY-N6801). This product is intended for research and analytical applications. Nivalenol, a trichothecene mycotoxin that can be produced by Fusarium graminearum, is a fungal metabolite present in agricultural product. Nivalenol modulates apoptotic pathway, cell cycle regulation, Bax, ERK, caspase-3, and poly-ADP-ribose synthase activity in macrophages. Nivalenol inhibits ribosomal peptidyltransferase site, protein synthesis, DNA synthesis, and cell proliferation. Nivalenol induces late-stage apoptotic morphological changes, reduces cellular metabolism, and decreases cell proliferation in erythroleukemia cells. Nivalenol induces lymphocyte apoptosis in murine thymus, spleen, and Peyer's patches. Nivalenol can be used for the research of erythroleukemia. | ||||||||||||||||||||
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Nivalenol-13C15 | Nivalenol-13C15 is the 13C labeled Nivalenol (HY-N6801). Nivalenol, a trichothecene mycotoxin that can be produced by Fusarium graminearum, is a fungal metabolite present in agricultural product. Nivalenol modulates apoptotic pathway, cell cycle regulation, Bax, ERK, caspase-3, and poly-ADP-ribose synthase activity in macrophages. Nivalenol inhibits ribosomal peptidyltransferase site, protein synthesis, DNA synthesis, and cell proliferation. Nivalenol induces late-stage apoptotic morphological changes, reduces cellular metabolism, and decreases cell proliferation in erythroleukemia cells. Nivalenol induces lymphocyte apoptosis in murine thymus, spleen, and Peyer's patches. Nivalenol can be used for the research of erythroleukemia. | |||||||||||||||||||||
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- [1]. Marzocco S, et al. Pro-apoptotic effects of nivalenol and deoxynivalenol trichothecenes in J774A.1 murine macrophages. Toxicol Lett. 2009;189(1):21-26. [Content Brief]
- [2]. Minervini F, et al. Toxicity and apoptosis induced by the mycotoxins nivalenol, deoxynivalenol and fumonisin B1 in a human erythroleukemia cell line. Toxicol In Vitro. 2004;18(1):21-28. [Content Brief]
- [3]. Aupanun S, et al. Individual and combined mycotoxins deoxynivalenol, nivalenol, and fusarenon-X induced apoptosis in lymphoid tissues of mice after oral exposure. Toxicon. 2019;165:83-94. [Content Brief]
