Molecular Formula | C16H24O4 |
Molar Mass | 280.36 |
Density | 1.108±0.06 g/cm3(Predicted) |
Melting Point | 200-205 °C |
Boling Point | 492.7±45.0 °C(Predicted) |
Flash Point | 87 °C |
Water Solubility | Soluble in dimethylsulfoxide, dichloromethane and ethanol. Slightly soluble in water. |
Solubility | methanol: 10 mg/mL, clear, colorless to faintly yellow |
Vapor Presure | 0.56 hPa ( 20 °C) |
Appearance | Morphological Crystalline Powder |
Color | White to almost white |
Merck | 13,1355 |
BRN | 25191 |
pKa | 12.92±0.60(Predicted) |
Storage Condition | Sealed in dry,Store in freezer, under -20°C |
Stability | Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 1 month. |
MDL | MFCD12913297 |
Physical and Chemical Properties | Bioactive Brefeldin A acts on HCT 116 cells, inhibits lactone antibiotics and ATPase, acts on protein transport (protein transport),IC50 is 0.2 μM, and induces cancer cell differentiation and apoptosis. It can also improve the repair efficiency of homologous recombination and is an enhancer for HDR CRISPR-mediated. Brefeldin A is also an inhibitor of autophagy and mitochondrial autophagy. |
Use | Use Brefeldin A, a commonly used protein transport inhibitor, specifically and reversibly blocks protein transport from the endoplasmic reticulum (ER) to the Golgi apparatus. After Brefeldin A treatment, the Golgi apparatus will be quickly destroyed and fused to the endoplasmic reticulum. The process is energy, temperature and microtubule dependent. In mammals and yeasts, the inhibition of protein transport from the endoplasmic reticulum to the Golgi apparatus by Brefeldin A may be achieved through a class of GTP-exchange factors that can activate Afr1p GTPase. Arf1p forms transport vesicles (transport vesicles) in cell intima by recruiting coat proteins |
Risk Codes | R22 - Harmful if swallowed R25 - Toxic if swallowed R36/37/38 - Irritating to eyes, respiratory system and skin. R20/21/22 - Harmful by inhalation, in contact with skin and if swallowed. |
Safety Description | S24/25 - Avoid contact with skin and eyes. S45 - In case of accident or if you feel unwell, seek medical advice immediately (show the label whenever possible.) S36 - Wear suitable protective clothing. S26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. |
UN IDs | UN 2811 6.1/PG 3 |
WGK Germany | 3 |
RTECS | GY8410000 |
HS Code | 29411090 |
Toxicity | LD50 i.p. in mice: >200 mg/kg (Haerri) |
Target
Target Value
ATPase (HCT 116) 0.2 μM
in vitro studies
Brefeldin A is a fungal metabolite that inhibits the transmission between the endoplasmic reticulum and the Golgi apparatus, Brefeldin A causes damage to the distribution of membrane proteins. Brefeldin A treated HCT 116 human colon cancer cells and observed morphological changes, indicating cell differentiation. Brefeldin A acts on tumor cells and exerts its cytotoxic effect mainly by inducing differentiation and apoptosis. The detection strip was treated with 20 μg/mL Brefeldin A for 6 hours, and the Bradykinin-induced relaxation was completely abolished in the presence of 10mM Indomethacin and 30 μM L-NOARG. Abolition of Bradykinin-induced [Ca Brefeldin A] did not affect the spontaneous phospholipid-dependent binding of GTPS to myr-rARF1, but completely abolished catalytic exchange of retinal isotonic extract (RIE) with a concentration of 20 μg/mL Brefeldin A between 1 nM and 1 mM, and the semi-inhibitory concentration of 2 μM Brefeldin A was 2 μM. Brefeldin A inhibits multiple membrane transport pathways. Brefeldin A acts on Golgi membrane or brain cytoplasm to inhibit the specific guanine nucleotide exchange activity of ADP-ribosylation factor. Complete inhibition of Brefeldin A indicates that retinal extract contains ARF-specific guanine nucleotide exchange factor. Brefeldin A only partially inhibited retinal isotonic extract (RIE)-catalyzed GTPS released by ADP-ribosylation factor (ARFs), even at concentrations as high as 300 μM. Brefeldin A induces Golgi fusion with ER. Brefeldin A abolished the inhibitory effect of CERT inhibitor HPA-12. Brefeldin A treated CHO cells to increase the synthesis of sphingomyelin by 2 to 3 times. In addition to B- CLL cells, Brefeldin A also causes apoptosis of multiple myeloma (U266,NCI-H929),JURKAT,HeLa cells, leukemia (HL60,K562,BJAB), colon (HT-29), and prostate, and adenoid cystic tumor cells. HF4.9 and HF28RA cells were treated with 25 ng/mL Brefeldin A, which completely inhibited cell growth, while high doses of Brefeldin A (75 ng/mL) were required to completely inhibit HF1A3 cell growth. HF1A3, HF4.9 and HF28RA cells were treated with 50-75 ng/mL Brefeldin A and inhibited cell proliferation within 24 hours. This effect was dose-dependent. Brefeldin A can improve the efficiency of homologous recombination and is an enhancer of CRISPR-mediated HDR.