C18-Ceramide (d18:1/18:0)  (Synonyms: C18-Ceramide)

C18-Ceramide (d18:1/18:0) is a bioactive molecule with multiple functions in cells, not a traditional agonist or inhibitor targeting a single site. It can act on multiple cellular targets, such as proteins related to endoplasmic reticulum stress (e.g., ATF-4, XBP-1, CHOP), proteins in the PI3K/AKT signaling pathway, and SNARE complex proteins. It exerts activities like inducing cell death, promoting autophagy, and regulating exocytosis through mechanisms such as activating endoplasmic reticulum stress, inhibiting the PI3K/AKT signaling pathway, and affecting lipid raft - related functions. It can be used in research on the mechanism of neuronal injury in the field of neuroscience and in the treatment research of cancers such as glioma in the field of oncology^[1][2].

In the PC12 cell capacitance measurement experiment, C18-Ceramide (d18:1/18:0) (2 μM; transient) can significantly increase the cell membrane capacitance, indicating that it can promote exocytosis^[1].
In the PC12 cell total internal reflection fluorescence microscopy (TIRFM) experiment, C18-Ceramide (d18:1/18:0) (2 μM) can rapidly reduce the number of NPY-EGFP-labeled subcellular membrane vesicles, which undergo endocytosis by fusing with the cell membrane^[1].
In U251 and A172 glioma cells, C18-Ceramide (d18:1/18:0) (20 μM; 48 h) inhibits glioma cell viability and induces cell death^[2].
C18-Ceramide (d18:1/18:0) (20 μM; 48 h) activates endoplasmic reticulum stress and increases the mRNA and protein levels of ATF-4, XBP-1 (s) and CHOP^[2].
C18-Ceramide (d18:1/18:0) induced lethal autophagy, increased the punctate distribution and density of GFP-LC3, promoted the conversion of LC3B-I to LC3B-II and decreased the level of p62^[2].
C18-Ceramide (d18:1/18:0) inhibited the PI3K/AKT pathway and decreased the expression levels of PI3K and p-AKT (S473)^[2].
C18-Ceramide (d18:1/18:0) (20μM; co-treatment with VM-26 for 48h) increased the chemosensitivity of U251 and A172 cells to VM-26 (HY-13761), synergistically inhibited cell growth, and induced more apoptosis^[2].

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

In the rat Kainate injury model, C18-Ceramide (d18:1/18:0) has an increasing content in the brain after injury. C18-Ceramide (d18:1/18:0) might facilitate the exocytosis of glutamate from damaged neurons, thus propagating neuronal injury^[1].

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

565.95

C₃₆H₇₁NO₃

2304-81-6

Solid

White to off-white

CCCCCCCCCCCCCCCCCC(N[C@@H](CO)[C@H](O)/C=C/CCCCCCCCCCCCC)=O

Room temperature in continental US; may vary elsewhere.

* 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.

• [1]. Tang N, et al. Differential effects of ceramide species on exocytosis in rat PC12 cells. Exp Brain Res. 2007 Nov;183(2):241-7.  [Content Brief]

  [2]. Wang Z, et al. Overexpression of ceramide synthase 1 increases C18-ceramide and leads to lethal autophagy in human glioma. Oncotarget. 2017 Oct 23;8(61):104022-104036.  [Content Brief]