| Bioactivity | 2-Chlorohexadecanoic acid, an inflammatory lipid mediator, interferes with protein palmitoylation,induces ER-stress markers, reduced the ER ATP content, and activates transcription and secretion of IL-6 as well as IL-8.2-Chlorohexadecanoic acid disrupts the mitochondrial membrane potential and induces procaspase-3 and PARP cleavage.2-Chlorohexadecanoic acid can across blood-brain barrier (BBB) and compromises ER- and mitochondrial functions in the human brain endothelial cell line hCMEC/D3[1]. |
| Invitro | 2-Chlorohexadecanoic acid (2-ClHA; 10 μM; 4, 6 h) results phosphorylation of eIF2α starting 4 h post treatment, while total eIF2α levels remained unchanged incubation of hCMEC/D3 cells. 2-Chlorohexadecanoic acid increases expression of ATF4, a target gene of eIF2α[1]. 2-Chlorohexadecanoic acid (25 µM, 30 min) induces a decrease in the FRET ratio signal of ERAT by 40%, indicating significantly diminished [ATP]ER in cells that were treated with 2-Chlorohexadecanoic acid[1]. |
| Name | 2-Chlorohexadecanoic acid |
| CAS | 19117-92-1 |
| Formula | C16H31ClO2 |
| Molar Mass | 290.87 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Reference | [1]. Eva Bernhart, et al. 2-Chlorohexadecanoic acid induces ER stress and mitochondrial dysfunction in brain microvascular endothelial cells. Redox Biol. 2018 May;15:441-451. |