Cat. No.: HY-N3806

Enniatin B

Name: Enniatin B
Brand: MedChemExpress
SKU: HY-N3806
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Enniatin B is a Fusarium mycotoxin that acts as an ionophore to form cation-selective membrane channels, disrupt ion homeostasis and mitochondrial function, inhibit cell proliferation, and induce apoptosis, while modulating ERK, p38 MAPK, and STAT3 signaling pathways. Enniatin B is used in research on atherosclerosis, hypercholesterolemia, cervical cancer, and colon adenocarcinoma.

For research use only. We do not sell to patients.

Purity : 99.86%
CAS No.: 917-13-5
Formula: C₃₃H₅₇N₃O₉
Molecular Weight:639.82

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

Enniatin B Chemical Structure

CAS No.: 917-13-5

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Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
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- In Vitro
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Biological Activity

Description

IC₅₀ & Target

^[11]

ERK

p38 MAPK

STAT3

All ERK Isoforms :

All p38 MAPK Isoforms :

All STAT Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
BALB/3T3	ED₅₀	8.4 μM	Reduction of intracellular ATP levels in mouse embryo fibroblast Balb 3T3 (clone A31) cells incubated for 24 h measured by ViaLight Plus ATP bioassay. Reduction of intracellular ATP levels in mouse embryo fibroblast Balb 3T3 (clone A31) cells incubated for 24 h measured by ViaLight Plus ATP bioassay.	27163883
HepG2	ED₅₀	2.9 μM	Reduction of intracellular ATP levels in human hepatocellular carcinoma HepG2 cells incubated for 24 h measured by ViaLight Plus ATP bioassay. Reduction of intracellular ATP levels in human hepatocellular carcinoma HepG2 cells incubated for 24 h measured by ViaLight Plus ATP bioassay.	27163883
BALB/3T3	ED₅₀	4.24 μM	Inhibition of cell proliferation (DNA synthesis) in mouse embryo fibroblast Balb 3T3 cells incubated for 24 h measured by BrdU ELISA chemiluminescent assay. Inhibition of cell proliferation (DNA synthesis) in mouse embryo fibroblast Balb 3T3 cells incubated for 24 h measured by BrdU ELISA chemiluminescent assay.	27163883
HepG2	ED₅₀	0.50 μM	Inhibition of cell proliferation (DNA synthesis) in human hepatocellular carcinoma HepG2 cells incubated for 24 h measured by BrdU ELISA chemiluminescent assay. Inhibition of cell proliferation (DNA synthesis) in human hepatocellular carcinoma HepG2 cells incubated for 24 h measured by BrdU ELISA chemiluminescent assay.	27163883
Caco-2	IC50	10.0 μM	Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 3 h measured by neutral red assay. Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 3 h measured by neutral red assay.	29201864
Caco-2	IC50	2.1 μM	Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 24 h measured by neutral red assay. Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 24 h measured by neutral red assay.	29201864
Caco-2	IC50	6.3 μM	Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 24 h measured by WST-1 assay. Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 24 h measured by WST-1 assay.	29201864
Caco-2	IC50	1.4 μM	Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 72 h measured by neutral red assay. Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 72 h measured by neutral red assay.	29201864
Caco-2	IC50	11.7 μM	Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 72 h measured by neutral red assay in an independent study. Cytotoxicity against human colon adenocarcinoma Caco-2 cells incubated for 72 h measured by neutral red assay in an independent study.	29201864
HepG2	IC50	206.7 μM	Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by Alamar Blue assay (lower bound of range). Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by Alamar Blue assay (lower bound of range).	29201864
HepG2	IC50	435.9 μM	Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by Alamar Blue assay (upper bound of range). Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by Alamar Blue assay (upper bound of range).	29201864
HepG2	IC50	0.9 μM	Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by BrdU incorporation assay (lower bound of range). Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by BrdU incorporation assay (lower bound of range).	29201864
HepG2	IC50	1.1 μM	Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by BrdU incorporation assay (upper bound of range). Cytotoxicity against human hepatocarcinoma HepG2 cells incubated for 24 h measured by BrdU incorporation assay (upper bound of range).	29201864
CHO-K1	IC50	11.0 μM	Cytotoxicity against Chinese hamster ovary CHO-K1 cells incubated for 24 h measured by MTT assay. Cytotoxicity against Chinese hamster ovary CHO-K1 cells incubated for 24 h measured by MTT assay.	29201864
CHO-K1	IC50	2.80 μM	Cytotoxicity against Chinese hamster ovary CHO-K1 cells incubated for 72 h measured by MTT assay. Cytotoxicity against Chinese hamster ovary CHO-K1 cells incubated for 72 h measured by MTT assay.	29201864
HT-29	IC50	2.8 μM	Cytotoxicity against human colon adenocarcinoma HT-29 cells across 24 and 48 h exposure measured by MTT assay. Cytotoxicity against human colon adenocarcinoma HT-29 cells across 24 and 48 h exposure measured by MTT assay.	29201864
MRC5	IC50	1.9 μM	Cytotoxicity against human fetal lung fibroblast MRC-5 cells incubated for 24 h measured by Alamar Blue assay (lower bound of range). Cytotoxicity against human fetal lung fibroblast MRC-5 cells incubated for 24 h measured by Alamar Blue assay (lower bound of range).	29201864
MRC5	IC50	9.8 μM	Cytotoxicity against human fetal lung fibroblast MRC-5 cells incubated for 24 h measured by Alamar Blue assay (upper bound of range). Cytotoxicity against human fetal lung fibroblast MRC-5 cells incubated for 24 h measured by Alamar Blue assay (upper bound of range).	29201864
MRC5	IC50	3.6 μM	Cytotoxicity against human fetal lung fibroblast MRC-5 cells incubated for 24 h measured by BrdU assay (upper bound of range). Cytotoxicity against human fetal lung fibroblast MRC-5 cells incubated for 24 h measured by BrdU assay (upper bound of range).	29201864
V79	IC50	34 μM	Cytotoxicity against Chinese hamster fibroblast V79 cells incubated for 24 h measured by Alamar blue assay. Cytotoxicity against Chinese hamster fibroblast V79 cells incubated for 24 h measured by Alamar blue assay.	29201864
V79	IC50	2.5 μM	Cytotoxicity against Chinese hamster fibroblast V79 cells incubated for 48 h measured by Alamar blue assay. Cytotoxicity against Chinese hamster fibroblast V79 cells incubated for 48 h measured by Alamar blue assay.	29201864
V79	IC50	4.4 μM	Cytotoxicity against Chinese hamster fibroblast V79 cells incubated for 48 h measured by neutral red assay. Cytotoxicity against Chinese hamster fibroblast V79 cells incubated for 48 h measured by neutral red assay.	29201864
V79	IC50	36 μM	Cytotoxicity against Chinese hamster fibroblast V79 cells measured by neutral red assay in an independent study (upper bound of range). Cytotoxicity against Chinese hamster fibroblast V79 cells measured by neutral red assay in an independent study (upper bound of range).	29201864
V79	IC50	4 μM	Cytotoxicity against Chinese hamster fibroblast V79 cells measured by neutral red assay in an independent study (lower bound of range). Cytotoxicity against Chinese hamster fibroblast V79 cells measured by neutral red assay in an independent study (lower bound of range).	29201864
V79	IC50	43 μM	Cytotoxicity against Chinese hamster fibroblast V79 cells measured by BCA protein content assay (upper bound of range). Cytotoxicity against Chinese hamster fibroblast V79 cells measured by BCA protein content assay (upper bound of range).	29201864
V79	IC50	3.9 μM	Cytotoxicity against Chinese hamster fibroblast V79 cells measured by BCA protein content assay (lower bound of range). Cytotoxicity against Chinese hamster fibroblast V79 cells measured by BCA protein content assay (lower bound of range).	29201864
RAW264.7	IC50	2.6 μM	Cytotoxicity against murine macrophage RAW 264.7 cells incubated for 24 h measured by Alamar blue assay. Cytotoxicity against murine macrophage RAW 264.7 cells incubated for 24 h measured by Alamar blue assay.	29201864
RAW264.7	IC50	4.7 μM	Cytotoxicity against murine macrophage RAW 264.7 cells incubated for 24 h measured by neutral red assay. Cytotoxicity against murine macrophage RAW 264.7 cells incubated for 24 h measured by neutral red assay.	29201864
BALB/3T3	ED₅₀	11 μM	Induction of apoptosis in mouse embryo fibroblast Balb 3T3 cells incubated for 24 h. Induction of apoptosis in mouse embryo fibroblast Balb 3T3 cells incubated for 24 h.	29201864
Caco-2	EC50	10 μM	Cytotoxicity measured as reduction in lysosomal activity in human colon adenocarcinoma Caco-2 cells after 3 h of exposure by Neutral Red assay. Cytotoxicity measured as reduction in lysosomal activity in human colon adenocarcinoma Caco-2 cells after 3 h of exposure by Neutral Red assay.	22731695
Caco-2	EC50	2.1 μM	Cytotoxicity measured as reduction in lysosomal activity in human colon adenocarcinoma Caco-2 cells after 24 h of exposure by Neutral Red assay. Cytotoxicity measured as reduction in lysosomal activity in human colon adenocarcinoma Caco-2 cells after 24 h of exposure by Neutral Red assay.	22731695
V79	IC50	4.0 μM	Cytotoxicity against Chinese hamster lung V79 cells incubated for 48 h measured by neutral red uptake assay. Cytotoxicity against Chinese hamster lung V79 cells incubated for 48 h measured by neutral red uptake assay.	19360736
V79	IC50	36.0 μM	Cytotoxicity against Chinese hamster lung V79 cells incubated for 24 h measured by neutral red uptake assay. Cytotoxicity against Chinese hamster lung V79 cells incubated for 24 h measured by neutral red uptake assay.	19360736
V79	IC₂₀	1.5 μM	Cytotoxicity against Chinese hamster lung V79 cells incubated for 48 h measured by neutral red uptake assay. Cytotoxicity against Chinese hamster lung V79 cells incubated for 48 h measured by neutral red uptake assay.	19360736
V79	IC₂₀	2.1 μM	Cytotoxicity against Chinese hamster lung V79 cells incubated for 24 h measured by neutral red uptake assay. Cytotoxicity against Chinese hamster lung V79 cells incubated for 24 h measured by neutral red uptake assay.	19360736
CCF-STTG1	IC50	8.9 μM	Cytotoxicity against human astrocytoma CCF-STTG1 cells assessed as reduction in cell viability incubated for 48 h by CCK-8 assay with WST-8 reduction measured at 457 nm. Cytotoxicity against human astrocytoma CCF-STTG1 cells assessed as reduction in cell viability incubated for 48 h by CCK-8 assay with WST-8 reduction measured at 457 nm.	29768483
Hep3B	IC50	3.38 μM	Growth inhibition of human Hep3B hepatocellular carcinoma cells incubated for 72 h assessed by MTT cell viability assay. Growth inhibition of human Hep3B hepatocellular carcinoma cells incubated for 72 h assessed by MTT cell viability assay.	25557295
CAKI-2	IC50	> 10 μM	Growth inhibition of human Caki-2 renal carcinoma cells incubated for 72 h assessed by MTT cell viability assay. Growth inhibition of human Caki-2 renal carcinoma cells incubated for 72 h assessed by MTT cell viability assay.	25557295
KB 3-1	IC50	3.72 μM	Growth inhibition of human KB-3-1 cervical carcinoma cells incubated for 72 h assessed by MTT cell viability assay. Growth inhibition of human KB-3-1 cervical carcinoma cells incubated for 72 h assessed by MTT cell viability assay.	25557295
Ca-Ski	IC50	3.38 μM	Growth inhibition of human CaSki cervical carcinoma cells incubated for 72 h assessed by MTT cell viability assay. Growth inhibition of human CaSki cervical carcinoma cells incubated for 72 h assessed by MTT cell viability assay.	25557295
HUVEC	IC50	7.7 μM	Viability inhibition of human umbilical vein endothelial cells incubated for 48 h. Viability inhibition of human umbilical vein endothelial cells incubated for 48 h.	25557295

In Vitro

Enniatin B (EnnB) (1.5-100 μM; 24 h) effectively reduces cellular ATP levels in Balb 3T3 and HepG2 cells in cell viability assays without disrupting plasma membrane integrity, with ED₅₀ values of 8.4 μM and 2.9 μM, respectively^[1].
Enniatin B (3-12 μM; 24 h) effectively inhibits the proliferation of Balb 3T3 and HepG2 cells in cell proliferation assays, with ED₅₀ values of 4.24 μM and 0.50 μM, respectively^[1].
Enniatin B (11-45 μM; 24-48 h) induces a slight dose-dependent increase in early apoptotic Balb 3T3 cells, with the majority of cells remaining intact^[1].
Enniatin B (0.00156-15.6 μM; 48 h) shows no specific agonistic or antagonistic effects on the transcriptional activity of estrogen, androgen, progesterone, or glucocorticoid receptors in reporter gene assays after 48 h^[3].
Enniatin B (0.1-10 μM; 48 h) reduces the viability of CCF-STTG1 human astrocytoma cells with an IC₅₀ of 8.9 μM; at concentrations above 5 μM, it moderately reduces the viability of primary porcine brain capillary endothelial cells; and after 48 h of treatment, it has no effect on the viability of HBMEC human brain microvascular endothelial cells at concentrations up to 10 μM^[10].
Enniatin B (0.1-2.5 μM; 48 h) induces a 2.7-fold increase in caspase-3 activity in CCF-STTG1 human astrocytoma cells after 48 h of treatment at a concentration of 2.5 μM, indicating activation of the apoptotic signaling pathway^[10].
Enniatin B (10 μM; 4 h) induces widespread downregulation of genes related to metabolism and mitochondrial structure in rat primary hepatocytes, including complex I subunits Ndufs1, Ndufs4, and Ndufs8, which is consistent with the manifestations of mitochondrial dysfunction and energy depletion^[1].
Enniatin B exhibits cytotoxic effects on human HepG2 cells, with potency varying widely depending on the assay method (ED₅₀ of 0.50 μM by BrdU ELISA and IC₅₀ greater than 435.9 μM by Alamar Blue)^[2].
Enniatin B (3 h) induces ROS production in human Caco-2 cells through a mitochondria-mediated cytotoxic pathway^[2].
Enniatin B (48 h) induces G₀/G₁ phase cell cycle arrest in human HepG2 cells^[2].
Enniatin B (1.25-10 μM; 24 h) induces G0/G1 phase cell cycle arrest in mouse RAW 264.7 macrophages^[2].
Enniatin B (3 μM; 72 h) induces G2/M phase cell cycle arrest in human Caco-2 cells, accompanied by a decrease in S phase cells and accumulation of cells in the SubG0/G1 phase^[2].
Enniatin B (48 h) induces apoptosis and necrotic cell death in human Caco-2 cells^[2].
Enniatin B (1.5-3.0 μM; 48 h) induces apoptosis in human HepG2 cells without causing necrosis^[2].
Enniatin B (0.66 μM; 2.5-30 min) undergoes extensive phase I metabolism via oxidation and N-demethylation in rat, dog, and human liver microsomes, producing 12 identified metabolites, with species-dependent metabolic profiles, and the intrinsic clearance in dog liver microsomes is approximately 7-fold higher than that in rat and human liver microsomes^[7].
Enniatin B (0.1-20 μM; 4 h) shows no mutagenicity up to cytotoxic concentrations of 20 μM in the HPRT assay in V79 cells in the presence and absence of rat liver S9 metabolic activation^[8].
Enniatin B (0.1-100 μM; 3-18 h) does not induce significant DNA strand breaks or oxidative DNA base damage in V79 cells, as determined by standard and FPG-modified alkaline comet assays^[8].
Enniatin B (up to 10 μM; 18 h) does not induce micronuclei in V79 cells, indicating a lack of clastogenic and aneugenic activity^[8].
Enniatin B (1 μM; 24 h) induces nuclear fragmentation, a marker of apoptosis, in approximately 10% of V79 cells^[8].
Enniatin B (0.1-2.5 μM; 48 h) does not induce significant LDH leakage in CCF-STTG1 human astrocytoma cells at concentrations up to 2.5 μM after 48 h of treatment, suggesting that necrosis is not the primary mode of cell death^[10].
Enniatin B (0.01-100 μM; 48 h) reduces the viability of H295R cells in a dose-dependent manner, with viability decreasing by 37% after 48 h of treatment at 100 μM^[3].
Enniatin B (0.01-100 μM; 48 h) reduces the viability of unstimulated and LH-stimulated neonatal porcine Leydig cells by approximately 20%^[3].
Enniatin B (0.00156-15.6 μM; 48 h) reduces the viability of TARM-Luc, TM-Luc, and TGRM-Luc reporter gene cell lines after 48 h treatment at 15.6 μM, with minimal effect on MMV-Luc cells^[3].
Enniatin B (30 min pre-incubation with inhibitors), when combined with MEK1/2 or p38 MAPK inhibitors, induces enhanced cytotoxicity in KB-3-1 cervical cancer cells, suggesting that both ERK and p38 pathways promote cell survival under Enniatin B treatment^[11].
Enniatin B (2-3 μM; 48 h), when combined with pharmacological p38 MAPK inhibition, induces decreased Hsp27 phosphorylation levels in KB-3-1 cervical cancer cells^[11].
Enniatin B (0.1-25 μM; 24-72 h) induces S phase arrest, a decreased G₀/G₁ phase proportion, and apoptosis in H295R cells in a time- and dose-dependent manner, with an apoptosis rate of 32.2% after 72 h of treatment at 25 μM^[3].
Enniatin B (0.01-100 μM; 48 h) decreases progesterone, testosterone, and cortisol production in H295R cells, while estradiol levels remain unchanged^[3].
Enniatin B (10 μM; 48 h) modulates the expression of 12 out of 16 steroidogenesis-related genes in H295R cells after 48 h of treatment, with downregulation of early pathway genes (HMGR, StAR, CYP11A, HSD3B2, CYP17A1) and upregulation of other steroidogenic and biotransformation genes^[3].
Enniatin B (0.01-100 μM; 48 h) reduces estradiol and testosterone production in LH-stimulated neonatal porcine Leydig cells, with minimal effects on unstimulated cells^[3].
Enniatin B (56 pM-437.2 μM; 3-24 h) effectively impairs lysosomal function in Caco-2 cells in a time- and concentration-dependent manner, with a 24 h EC₅₀ of 2.1 μM, without affecting metabolic activity or membrane integrity at the tested concentrations^[5].
Enniatin B (1-50 μM; 3-24 h) induces rapid and concentration-dependent lysosomal membrane permeabilization in Caco-2 cells, with damage detectable as early as 3 h and pronounced disruption at 24 h^[5].
Enniatin B (1-25 μM; 24 h) decreases Caco-2 cell proliferation in a concentration-dependent manner, with a 50% reduction in proliferation at 25 μM after 24 h, accompanied by progressive morphological changes and cell detachment^[5].
Enniatin B (1-25 μM; 24 h) causes a slight but detectable G₂/M phase cell cycle arrest in Caco-2 cells after 24 h treatment at 25 μM, without leading to significant accumulation of sub-G₁ phase cells^[5].
Enniatin B (24 h) as a single agent has only a minimal effect on DNA synthesis in KB-3-1 cervical cancer cells^[11].
Enniatin B (24-48 h) induces moderate G₀/G₁ phase cell cycle arrest in KB-3-1 cervical cancer cells, and this effect is more pronounced after 48 h of treatment^[11].
Enniatin B (1-25 μM; 24 h) predominantly induces necrotic cell death in Caco-2 cells in a dose-dependent manner, with necrotic cells accounting for approximately 13% after 24 h treatment at 25 μM, and with minimal apoptosis^[5].
Enniatin B (5-10 μM; 3-24 h) induces dose-dependent changes in mitochondrial membrane permeability in Caco-2 cells, an effect detectable as early as 3 h and more pronounced at 24 h, which is not mediated by cathepsins^[5].
Enniatin B (1-25 μM; 3-24 h) induces a 2.4-fold increase in intracellular ROS levels in Caco-2 cells after 24 h treatment at 5 μM, an effect that is completely inhibited by the antioxidant ascorbic acid^[5].
Enniatin B (1-10 μM; 24 h) induces the release of cathepsins B and D from lysosomes into the cytosol of Caco-2 cells in a concentration-dependent manner after 24 h of exposure, with altered processing, which is consistent with lysosomal membrane permeabilization^[5].
Enniatin B (5 μM; 24 h) treatment leads to the appearance of mature caspases (caspase-14, -6, -3) and the pro-apoptotic proteins Bax and Bid in the cytoplasm of Caco-2 cells, which is consistent with the activation of cell death pathways^[5].
Enniatin B (0.009-100 μM; 24-72 h) exerts potent multiparametric hepatotoxic effects in Hep-G2 cells, with significant toxicity observed at 0.9 μM after 24 h and 72 h of exposure^[6].
Enniatin B (100 nM-100 μM; 20 min preincubation, 2-day culture) is not mutagenic to Salmonella typhimurium strains TA 98, TA 100, TA 102, and TA 104 in the presence or absence of rat liver S9 metabolic activation, with the highest tested toxic concentration being 100 μM^[8].
Enniatin B (4-10 μM; 24 h) exhibits potent cytotoxicity against human umbilical cord blood-derived immature dendritic cells, mature dendritic cells, and macrophages, with IC₅₀ values of 1.6 μM, 2.6 μM, and 2.5 μM, respectively^[9].
Enniatin B (1-1.3 μM; 5 days) does not alter CD1a expression during the differentiation of human umbilical cord blood monocytes into immature dendritic cells at concentrations of 1 μM and 1.3 μM^[9].
Enniatin B (1-1.3 μM; 5 days) does not affect the endocytic capacity during the differentiation of human umbilical cord blood monocytes into immature dendritic cells at concentrations of 1 μM and 1.3 μM^[9].
Enniatin B (0.5-1 μM; 6 days) reduces the endocytic capacity during the differentiation of human umbilical cord blood monocytes into macrophages^[9].
Enniatin B (0.5-1 μM; 6 days) does not alter respiratory burst activity during the differentiation of human umbilical cord blood monocytes into macrophages at concentrations of 0.5 μM and 1 μM^[9].
Enniatin B (0.5-1 μM; 6 days) upregulates CD71 expression in a dose-dependent manner during the differentiation of human umbilical cord blood monocytes into macrophages, while the expression of CD11a, HLA-DR, CD80, and CD54 remains unchanged^[9].
Enniatin B (1-2 μM; 2 days) downregulates the maturation markers CD80, CD86, and CCR7 during Lipopolysaccharides, from E. coli O55:B5 (HY-D1056)-induced maturation of human cord blood-derived dendritic cells at 2 μM, while HLA-DR expression remains unaffected^[9].
Enniatin B (1-2 μM; 2 days) increases IL-10 secretion during LPS-induced maturation of human umbilical cord blood-derived dendritic cells^[9].
Enniatin B (0.5-1 μM; 6 days) does not alter TNF-α secretion during the differentiation of human umbilical cord blood monocytes into macrophages at concentrations of 0.5 μM and 1 μM^[9].
Enniatin B (72 h) inhibits the viability of multiple human cancer cell lines with low micromolar potency, with IC₅₀ values ranging from 1.74 μM (HTB-31 cervical cancer) to > 10 μM (Caki-2 renal cell carcinoma)^[11].
Enniatin B (3 μM; 24 h) induces mitochondrial membrane depolarization and increases the proportion of late apoptosis/necrosis in KB-3-1 cervical cancer cells after 24 h of treatment^[11].
Enniatin B (1-3 μM; 48 h) modulates the expression of apoptosis-related proteins in KB-3-1 cervical cancer cells, inducing caspase-7 activation, PARP cleavage, upregulation of the pro-apoptotic genes bak and bim, and downregulation of the pro-survival genes bcl-xL and Mcl-1^[11].
Enniatin B (1-3 μM; 48 h) modulates the expression of cell cycle proteins in KB-3-1 cervical cancer cells, and its mode of action is consistent with G₀/G₁ phase cell cycle arrest^[11].
Enniatin B (1-3 μM; 48 h) modulates multiple MAPK signaling pathways in KB-3-1 cervical cancer cells, inhibiting ERK phosphorylation while strongly activating p38 MAPK and its downstream target CREB, and reducing STAT3 phosphorylation levels^[11].
Enniatin B (2.5 μM; 20 h) effectively inhibits capillary-like tube formation in human umbilical vein endothelial cells at subtoxic concentrations^[11].
Enniatin B (4 μM; 15 h) strongly inhibits VEGF-induced migration of human umbilical vein endothelial cells^[11].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay^[1]

Cell Line:

Mouse embryo fibroblast Balb 3T3 (clone A31) cells, human hepatocellular carcinoma HepG2 cells
Concentration:

1.5, 3.1, 6.25, 12.5, 25, 50, 100 μM
Incubation Time:

24 h
Result:

Reduced intracellular ATP levels in Balb 3T3 cells in a steep, dose-dependent manner with an ED₅₀ of 8.4 μM; concentrations below 3 μM had no effect.
Detected no adenylate kinase leakage through the plasma membrane in Balb 3T3 cells at the tested concentrations, indicating preserved membrane integrity.
Reduced intracellular ATP levels in HepG2 cells in a dose-dependent pattern with an ED₅₀ of 2.9 μM.

Cell Proliferation Assay^[1]

Cell Line:

Mouse embryo fibroblast Balb 3T3 cells, human hepatocellular carcinoma HepG2 cells
Concentration:

3, 4, 5, 6, 7, 8, 9, 10, 11, 12 μM
Incubation Time:

24 h
Result:

Caused a marked decline in DNA synthesis in both cell lines within a narrow concentration range.
Yielded an estimated ED₅₀ for inhibition of proliferation of 4.24 μM in Balb 3T3 cells; concentrations under 3.5 μM showed no inhibition.
Yielded an estimated ED₅₀ for inhibition of proliferation of 0.50 μM in HepG2 cells.

Apoptosis Analysis^[1]

Cell Line:

Mouse embryo fibroblast Balb 3T3 cells
Concentration:

11, 22.5, 45 μM
Incubation Time:

24, 48 h
Result:

Slightly increased the proportion of early apoptotic Balb 3T3 cells in a dose-dependent manner following 24 h of exposure: from 0.3% in negative control cells to 1.25% at 11 μM, 2.5% at 22.5 μM, and 4.4% at 45 μM.
Showed a rising trend in the proportion of late apoptotic/necrotic cells with increasing concentration after 24 h.
Resulted in 96.6% intact cells at 11 μM, 91.0% at 22.5 μM, and 84.3% at 45 μM after 24 h, compared to 86% in negative control samples.
Induced a statistically significant increase in early apoptotic cells from 0.0% in controls to 3.6% at 45 μM after 48 h of exposure.

Real Time qPCR^[1]

Cell Line:

Cryopreserved rat primary hepatocytes
Concentration:

10 μM
Incubation Time:

1, 4 h
Result:

Confirmed the microarray findings for Ndufs4 and Timm21, showing downregulated relative expression of both genes following exposure.
Showed no statistically significant change in expression of caspase genes (Casp1, Casp3, Casp7, Casp9) compared to unexposed controls.

Cell Cycle Analysis^[2]

Cell Line:

Human colon adenocarcinoma Caco-2 cells
Concentration:

3 μM
Incubation Time:

72 h
Result:

Induced cell cycle arrest in the G2/M phase in Caco-2 cells after 72 h of exposure, with a significant increase in G2/M cell number compared to control.
Decreased the S phase cell population and increased the SubG0/G1 population.

Apoptosis Analysis^[2]

Cell Line:

Human hepatocarcinoma HepG2 cells
Concentration:

1.5, 3.0 μM
Incubation Time:

48 h
Result:

Caused apoptosis in HepG2 cells after 48 h of exposure, with enniatin B identified as more toxic than enniatin A.
No necrotic pathway was observed.

Cell Viability Assay^[3]

Cell Line:

human adrenocortical carcinoma H295R cells
Concentration:

0.01, 0.1, 1, 10, 100 μM
Incubation Time:

48 h
Result:

Induced an increase in cell viability up to the 1 μM dose, followed by a dose-dependent decrease at higher concentrations.
Caused an average reduction in viable cells of 37% compared to control cells.

Cell Cycle Analysis^[3]

Cell Line:

human adrenocortical carcinoma H295R cells
Concentration:

0.1, 1, 10, 15, 25 μM
Incubation Time:

24, 48, 72 h
Result:

With the exception of the 24 h exposure, led to a dose-dependent reduction of cells in the G₀/G₁ phase.
The reduction in G₀/G₁ phase cells was significant at concentrations > 10 μM after 72 h of exposure.
Increased the proportion of cells in S phase across all exposure durations.
Concentrations > 15 μM significantly increased the percentage of apoptotic (sub-G₀) cells.
At 25 μM, the apoptotic cell proportions were approximately 11%, 24.6%, and 32.2% after 24 h, 48 h, and 72 h exposures, respectively.

Real Time qPCR^[3]

Cell Line:

human adrenocortical carcinoma H295R cells
Concentration:

10 μM
Incubation Time:

48 h
Result:

Significantly modulated twelve of the sixteen analyzed genes.
Significantly downregulated HMGR, StAR, CYP11A, HSD3B2, and CYP17A1.
Significantly upregulated CYP1A1, MC2R, NR0B1, CYP21A2, CYP11B1, CYP11B2, and CYP19.
Did not significantly alter expression levels of EPHX, NR5A1, HSD17B1, and HSD17B4.

Cell Viability Assay^[3]

Cell Line:

primary neonatal porcine Leydig cells (both unstimulated and LH-stimulated)
Concentration:

0.01, 0.1, 1, 10, 100 μM
Incubation Time:

48 h
Result:

At 0.01-10 μM, caused no significant difference in Leydig cell viability under either unstimulated or LH-stimulated condition.
At 100 μM, significantly reduced cell viability, with average viabilities of 80% in unstimulated cells and 79% in LH-stimulated cells compared to controls.

Cell Viability Assay^[3]

Cell Line:

four human mammary gland reporter gene cell lines (MMV-Luc, TARM-Luc, TM-Luc, TGRM-Luc)
Concentration:

0.00156, 0.0156, 0.156, 1.56, 15.6 μM
Incubation Time:

48 h
Result:

Caused no significant difference in cell viability in any of the four RGA cell lines.
At 15.6 μM, caused a significant decrease in cell viability (37-50% reduction) in TARM-Luc, TM-Luc, and TGRM-Luc cell lines, while the MMV-Luc cell line showed a non-significant trend toward reduced viability (approximately 7% reduction).

Cell Proliferation Assay^[5]

Cell Line:

Human colon adenocarcinoma Caco-2 cells
Concentration:

1, 5, 10, 25 μM
Incubation Time:

24 h
Result:

Decreased cell proliferation in a concentration-dependent manner.
Reduced viability to 85% of control at 1 μM.
Reduced viability to 67% of control at 5 μM.
Reduced viability to 69% of control at 10 μM.
Reduced viability to 50% of control at 25 μM.
Caused only minimal cell rounding and floating at 1 μM.
Induced progressive cell detachment, loss of cell-cell contacts, and altered morphology at concentrations above 5 μM, most pronounced at 25 μM.
Showed partially reversed proliferation decrease in the presence of 40 μM pepstatin A.
Did not show reversed proliferation decrease in the presence of 20 μM E-64d.

Cell Cycle Analysis^[5]

Cell Line:

Human colon adenocarcinoma Caco-2 cells
Concentration:

1, 5, 10, 25 μM
Incubation Time:

24 h
Result:

Induced a slight shift in cell cycle distribution with a noticeable increase in the G₂/M phase population.
Resulted in 31% of cells in G₂/M phase at 25 μM compared with 23% in untreated controls.
Did not cause a marked increase in the sub-G₁ population at any tested concentration.

Apoptosis Analysis^[5]

Cell Line:

Human colon adenocarcinoma Caco-2 cells
Concentration:

1, 5, 10, 25 μM
Incubation Time:

24 h
Result:

Induced cell death with a clear predominance of necrosis over apoptosis across the tested concentration range.
Increased the proportion of necrotic cells in a dose-dependent manner, reaching approximately 13% at 25 μM.
Resulted in at most 2% apoptotic cells at 1 μM, with apoptotic cell proportion decreasing at higher concentrations.
Produced less than 1% double-stained post-apoptotic necrotic cells at all concentrations.
Decreased the number of normal cells by approximately 12% with increasing concentration, matching the increase in necrotic cells.
Showed only a minimal decrease in the number of necrotic cells in the presence of ascorbic acid.

Immunofluorescence^[5]

Cell Line:

Human colon adenocarcinoma Caco-2 cells
Concentration:

10, 25, 50 μM (3 h); 1, 5, 10, 25 μM (24 h)
Incubation Time:

3, 24 h
Result:

Caused a dramatic decrease in LysoTracker Red fluorescence intensity after 24 h of exposure, indicating altered lysosomal acidification and function.
Induced initial increase in lysosome size followed by disintegration with increasing concentration.
Caused marked rupture of lysosomal membranes after only 3 h of treatment with 10 μM.
Produced extent of lysosomal damage at 25 μM comparable to that of the positive control L-leucyl-L-leucine methyl ester.

Western Blot Analysis^[5]

Cell Line:

Human colon adenocarcinoma Caco-2 cells
Concentration:

1, 5, 10 μM
Incubation Time:

24 h
Result:

Caused concentration-dependent changes in the levels of different cathepsin forms in the cytosolic fraction.
Increased signal intensities of cathepsin B at 27 kDa (mature heavy chain) and 37 kDa (procathepsin B) with higher concentrations.
Slightly decreased the 42 kDa preprocathepsin B signal of cathepsin B.
Increased the 33 kDa single-chain cathepsin B signal first at 1 μM then returned to control levels at 5 and 10 μM.
Increased the 48 kDa (double-glycosylated procathepsin D) signal of cathepsin D.
Barely changed the 46 kDa active single-chain signal of cathepsin D.
Considerably decreased the 42 kDa preprocathepsin D and 27 kDa mature heavy chain signals of cathepsin D.
Detected bands for procathepsin L (43 kDa) and single-chain cathepsin L (30 kDa) in the cytosol, with less unambiguous signals for cathepsin L.

Cell Cytotoxicity Assay^[6]

Cell Line:

human Hep-G2 hepatocellular carcinoma cells
Concentration:

0.009, 0.09, 0.9, 9, 13, 20, 30, 44, 67, and 100 μM
Incubation Time:

24, 72 h
Result:

Displayed a strong hepatotoxic response deviating significantly from control starting at 0.9 μM after 24 h of exposure.
Exerted the most pronounced effect on plasma membrane integrity, with concomitant effects on mitochondrial area/mass, mitochondrial membrane potential, decreased lysosomal activity, and reduced nuclear count after 24 h.
Showed a cytotoxicity response very similar to 24 h exposure, with no significant enhancement of toxicity with prolonged exposure after 72 h.
Exhibited greater cytotoxic potency than aflatoxin B1.

Apoptosis Analysis^[8]

Cell Line:

V79 Chinese hamster lung fibroblasts
Concentration:

1 μM
Incubation Time:

24 h
Result:

Induced clear nuclear fragmentation frequently in cultures treated for 24 h, with approximately 10% of all cells showing fragmented nuclei, a morphological feature of apoptotic cell death.

Cell Viability Assay^[9]

Cell Line:

human umbilical cord blood-derived immature dendritic cells, mature dendritic cells, and macrophages
Concentration:

10 μM (immature dendritic cells and macrophages); 4 μM (mature dendritic cells)
Incubation Time:

24 h
Result:

Showed cytotoxicity to all three cell types.
Left 18% of immature dendritic cells viable at 10 μM.
Left 30% of macrophages viable at 10 μM.
Left 33% of mature dendritic cells viable at 4 μM.
Exhibited an IC₅₀ of 1.6 μM for immature dendritic cells.
Exhibited an IC₅₀ of 2.6 μM for mature dendritic cells.
Exhibited an IC₅₀ of 2.5 μM for macrophages.

ELISA Assay^[9]

Cell Line:

human umbilical cord blood monocyte-derived mature dendritic cells
Concentration:

1, 2 μM
Incubation Time:

2 days
Result:

Increased IL-10 secretion to 753 pg/mL at 2 μM compared to the control level of 496 pg/mL.

ELISA Assay^[9]

Cell Line:

human umbilical cord blood monocyte-derived macrophages
Concentration:

0.5, 1 μM
Incubation Time:

6 days
Result:

Maintained TNF-α secretion similar to control levels at 0.5 μM and 1 μM.

Cell Viability Assay^[10]

Cell Line:

primary porcine brain capillary endothelial cells (PBCEC), human brain microvascular endothelial cells (HBMEC), human astrocytoma CCF-STTG1 cells
Concentration:

0.1, 1, 2.5, 5, 10 μM
Incubation Time:

48 h
Result:

Caused a decrease in viability at concentrations above 5 μM in PBCEC, with a minimum relative viability of 70% at 10 μM.
Showed no effect on viability across the 0.1 μM to 10 μM concentration range in HBMEC.
Produced strong cytotoxic effects at 5 μM and 10 μM in CCF-STTG1 astrocytoma cells, with an IC₅₀ of 8.9 μM.

Apoptosis Analysis^[10]

Cell Line:

human astrocytoma CCF-STTG1 cells
Concentration:

0.1, 1, 2.5 μM
Incubation Time:

48 h
Result:

Resulted in a 2.7-fold increase in caspase-3 activity compared to the solvent control at 2.5 μM.
Produced only minor differences relative to the control at lower concentrations.

Cell Cytotoxicity Assay^[10]

Cell Line:

human astrocytoma CCF-STTG1 cells
Concentration:

0.1, 1, 2.5 μM
Incubation Time:

48 h
Result:

Detected no significant increase in LDH release into the medium across the tested concentration range.

Apoptosis Analysis^[11]

Cell Line:

human KB-3-1 cervical carcinoma cells
Concentration:

3 μM
Incubation Time:

24 h
Result:

Increased the numbers of PI-permeable cells indicative of late apoptotic/necrotic cells compared to untreated controls.

Western Blot Analysis^[11]

Cell Line:

human KB-3-1 cervical carcinoma cells
Concentration:

1, 2, 3 μM
Incubation Time:

48 h
Result:

Caused concentration-dependent increases in cleaved PARP and cleaved caspase 7.
Upregulated the pro-apoptotic proteins bak and bim.
Reduced the pro-survival proteins bcl-xL and Mcl-1 at higher concentrations.
Left Bax protein levels largely unchanged across the concentration range.\nInduced concentration-dependent changes in cyclin expression consistent with the observed G₀/G₁ cell cycle distribution.\nCaused a concentration-dependent decrease in ERK phosphorylation.
Induced a strong concentration-dependent activation (phosphorylation) of p38 MAPK.
Induced a comparable activation pattern for the p38 downstream target CREB.
Significantly reduced phosphorylation of STAT3.
Induced phosphorylation of Hsp27 (a downstream target of p38).

Western Blot Analysis^[11]

Cell Line:

human KB-3-1 cervical carcinoma cells
Concentration:

2, 3 μM
Incubation Time:

48 h
Result:

Showed reduced phosphorylation of Hsp27 when cells were concomitantly treated with the p38 inhibitor SB203580.

Cell Migration Assay ^[11]

Cell Line:

human umbilical vein endothelial cells (HUVEC)
Concentration:

4 μM
Incubation Time:

15 h
Result:

Markedly impaired migration in VEGF-stimulated cells, with 75% of the initial scratch gap remaining open after 15 h, whereas VEGF-only treated cells nearly closed the wound.

Parmacokinetics

Species	Dose	Route	V_d	Serum Concentration	Brain Concentration	Bioavailability
Pig^[2]	0.05 mg/kg	p.o.	/	/	/	91 %
Chicken^[2]	0.2 mg/kg	p.o.	33.91 L/kg	/	/	/
Mice^[4]	5 mg/kg	i.p.	/	0.00045 μg/g	0.0001 g/kg	/

In Vivo

Enniatin B (5 mg/kg; i.p.; once daily; for 2 consecutive days) does not cause acute tissue damage in mice, but accumulates in lipophilic tissues^[2].
Enniatin B (1.25-40 mg/kg; i.p.; every 8 h) causes death in mice within 2 to 5 days at doses of 10 mg/kg and above, reduces body weight, and shows no anti-HIV activity in mice^[2].
Enniatin B (0.2 mg/kg; intravenous bolus; single dose) is widely distributed in broiler tissues, with an average volume of distribution of 33.91 L/kg^[2].
Enniatin B (0.05 mg/kg; oral bolus; single dose) exhibits a higher absorption extent than ENN B1, ENN A1, and ENN A in pigs^[2].
Enniatin B (1.03 mg/kg; p.o.), as a component of a mixture of four enniatins, produces no adverse effects in Wistar rats^[2].
Enniatin B (5 mg/kg; i.p.; once daily; for 2 consecutive days) is well tolerated in healthy SCID mice, accumulates mainly in the liver and fat, and is extensively metabolized into three phase I metabolites in the liver and intestine^[4].
Enniatin B (5 mg/kg; i.p.; once daily; for 9 consecutive days) is well tolerated in mice bearing KB-3-1 cervical cancer xenografts and accumulates in tumor tissue at a concentration of 2.8 μg/kg^[4].
Enniatin B (5 mg/kg; i.p.; once daily; for 14 days) as a single agent does not significantly reduce the growth of KB-3-1 cervical cancer xenografts in SCID mice^[11].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Broiler chickens^[2]
Dosage:

0.2 mg/kg
Administration:

bolus; single dose
Result:

Distributed readily to broiler chicken tissues.
Had a mean volume of distribution of 33.91 L/kg.

Animal Model:

strain not specified^[2]
Dosage:

0.05 mg/kg
Administration:

oral bolus; single dose
Result:

Showed higher absorption than ENN B1, ENN A1, and ENN A.

Animal Model:

CB-17 scid/scid (severe combined immunodeficiency) mice (male; 8 weeks old; average weight 25 g)^[4]
Dosage:

5 mg/kg
Administration:

i.p.; once daily; 2 consecutive days
Result:

Showed no apparent signs of toxicity including reduced food/fluid consumption, fatigue, or body weight alterations.
Exhibited intact tissue architecture in liver, lung, and kidneys with no acute or subchronic toxic damage, and no increase in mitotic numbers, proliferation rates, or apoptotic bodies.
Was detected in all tested tissues and serum but not in urine.
Reached concentrations of 2.9 μg/kg in liver, 0.1 μg/kg in kidney, 0.9 μg/kg in colon, 2.5 μg/kg in fat, 0.1 μg/kg in brain, 0.12 μg/kg in muscle, and 0.45 μg/kg in serum.
Was metabolized to three phase I metabolites (dioxygenated-Enniatin B, monodemethylated-Enniatin B, didemethylated-Enniatin B) in liver and colon.
Had metabolite concentrations in liver of 26.9 μg/kg for dioxygenated-Enniatin B, 0.7 μg/kg for monodemethylated-Enniatin B, and 1.0 μg/kg for didemethylated-Enniatin B.
Had metabolite concentrations in colon of 2.5 μg/kg for dioxygenated-Enniatin B, 0.6 μg/kg for monodemethylated-Enniatin B, and 2.45 μg/kg for didemethylated-Enniatin B.
Had no metabolites detected in serum, brain, muscle, or kidney.

Animal Model:

CB-17 scid/scid (severe combined immunodeficiency) mice (male; 8 weeks old; average weight 25 g; KB-3-1 human cervix carcinoma xenograft model)^[4]
Dosage:

5 mg/kg
Administration:

i.p.; once daily; 9 days
Result:

Showed no apparent signs of toxicity including reduced food/fluid consumption, fatigue, or body weight alterations throughout the 9-day treatment.
Exhibited intact tissue architecture in liver, lung, and kidneys with no acute or subchronic toxic damage.
Reached a concentration of 2.8 μg/kg in tumor tissue.
Reached a concentration of 5.4 μg/kg in serum.
Had no degradation products (metabolites) detected in the analyzed tumor tissues.

Animal Model:

CB-17 scid/scid (SCID) mice (male, 8 weeks old)^[11]
Dosage:

5 mg/kg
Administration:

i.p.; daily; 14 days
Result:

Produced tumor volume and tumor weight values at day 14 that were approximately equal to those of the solvent control group.

Chemical Information

CAS No. 917-13-5
Appearance Solid
Molecular Weight 639.82
Formula C₃₃H₅₇N₃O₉
Color White to off-white
SMILES

CC([C@](O1)([H])C(N([C@H](C(O[C@@H](C(N([C@](C(C)C)([H])C(O[C@H](C(C)C)C(N(C)[C@@H](C(C)C)C1=O)=O)=O)C)=O)C(C)C)=O)C(C)C)C)=O)C
Structure Classification
- Alkaloids
- Other Alkaloids
Initial Source
- Microorganisms
Fusarium spp.
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Solvent & Solubility

In Vitro:

DMSO : ≥ 10 mg/mL (15.63 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

* "≥" means soluble, but saturation unknown.

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

1.5629 mL

7.8147 mL

15.6294 mL

5 mM

0.3126 mL

1.5629 mL

3.1259 mL

10 mM

0.1563 mL

0.7815 mL

1.5629 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (340 KB)
SDS (480 KB)
- English - EN (480 KB)
- Français - FR (480 KB)
- Deutsch - DE (480 KB)
- Norwegian - NO (480 KB)
- Español - ES (480 KB)
- Swedish - SV (480 KB)
- Italian - IT (480 KB)
- Korean - KR (480 KB)
- Portuguese - PT (480 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Jonsson M, et al. Fusarium mycotoxin enniatin B: Cytotoxic effects and changes in gene expression profile. Toxicology in vitro : an international journal published in association with BIBRA. 2016 Aug;34:309-320.

[2]. Prosperini A, et al. A Review of the Mycotoxin Enniatin B. Frontiers in public health. 2017;5:304.

[3]. Kalayou S, et al. An investigation of the endocrine disrupting potential of enniatin B using in vitro bioassays. Toxicology letters. 2015 Mar 04;233(2):84-94.

[4]. Rodríguez-Carrasco Y, et al. Mouse tissue distribution and persistence of the food-born fusariotoxins Enniatin B and Beauvericin. Toxicology letters. 2016 Apr 15;247:35-44.

[5]. Ivanova L, et al. Lysosomes as a possible target of enniatin B-induced toxicity in Caco-2 cells. Chemical research in toxicology. 2012 Aug 20;25(8):1662-74.

[6]. Svingen T, et al. Enniatin B and beauvericin are common in Danish cereals and show high hepatotoxicity on a high-content imaging platform. Environmental toxicology. 2017 May;32(5):1658-1664.

[7]. Ivanova L, et al. In vitro phase I metabolism of the depsipeptide enniatin B. Analytical and bioanalytical chemistry. 2011 Jul;400(9):2889-901.

[8]. Behm C, et al. The Fusarium toxin enniatin B exerts no genotoxic activity, but pronounced cytotoxicity in vitro. Molecular nutrition & food research. 2009 Apr;53(4):423-30.

[9]. Ficheux AS, et al. Effects of beauvericin, enniatin b and moniliformin on human dendritic cells and macrophages: an in vitro study. Toxicon : official journal of the International Society on Toxinology. 2013 Sep;71:1-10. [Content Brief]

[10]. Krug I, et al. Transport of enniatin B and enniatin B1 across the blood-brain barrier and hints for neurotoxic effects in cerebral cells. PloS one. 2018;13(5):e0197406. [Content Brief]

[11]. Dornetshuber-Fleiss R, et al. The naturally born fusariotoxin enniatin B and sorafenib exert synergistic activity against cervical cancer in vitro and in vivo. Biochemical pharmacology. 2015 Feb 01;93(3):318-331.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.5629 mL	7.8147 mL	15.6294 mL	39.0735 mL
	5 mM	0.3126 mL	1.5629 mL	3.1259 mL	7.8147 mL
	10 mM	0.1563 mL	0.7815 mL	1.5629 mL	3.9073 mL
	15 mM	0.1042 mL	0.5210 mL	1.0420 mL	2.6049 mL

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Enniatin B

All ERK Isoforms

All p38 MAPK Isoforms

All STAT Isoforms