15-Hydroxypentadecanoic acid Reference: M1881-25 This odd numbered omega-hydroxy pentadecanoic acid is ideal as an internal standard for studies involving medium to longchain omega-hydroxy fatty acids.1 omega-Hydroxy C15:0 fatty acid and other omega-hydroxy fatty acids can be lactonized by certain enzymes into mono- and oligolactones.2 omega-Oxidation is a minor fatty acid pathway used for fatty acid metabolism and usually occurs in the smooth endoplasmic reticulum. Stimulation of omega-hydroxylation has been proposed as a method for treating X-linked adrenoleukodystrophy, a disease that is characterized by elevated levels of very long chain fatty acids.3 omega-Hydroxy fatty acids have an important role while acylated to various lipids. omega- Hydroxylated very long chain fatty acid (VLCFA) ceramides are vital to skin barrier functions and a deficiency of these lipids can cause death from water loss through the skin. In atopic dermatitis, a common skin disease, there are considerable deficiencies of omega-hydroxy long chain fatty acids acylated to ceramides and this may contribute to the severely damaged permeability barrier found in this disease.4
Methyl 15-hydroxypentadecanoate Reference: M1882-25 This odd numbered omega-hydroxy pentadecanoate methyl ester is ideal as an internal standard for studies involving medium to long-chain omega-hydroxy fatty acids.1 omega-Hydroxy C15:0 fatty acid and other omega-hydroxy fatty acids can be lactonized by certain enzymes into mono- and oligolactones.2 omega-Oxidation is a minor fatty acid pathway used for fatty acid metabolism and usually occurs in the smooth endoplasmic reticulum. Stimulation of omega-hydroxylation has been proposed as a method for treating X-linked adrenoleukodystrophy, a disease that is characterized by elevated levels of very long chain fatty acids.3 omega-Hydroxy fatty acids have an important role while acylated to various lipids. omega- Hydroxylated very long chain fatty acid (VLCFA) ceramides are vital to skin barrier functions and a deficiency of these lipids can cause death from water loss through the skin. In atopic dermatitis, a common skin disease, there are considerable deficiencies of omega-hydroxy long chain fatty acids acylated to ceramides and this may contribute to the severely damaged permeability barrier found in this disease.4
Methyl 27-hydroxyheptacosanoate Reference: M1883-25 This odd numbered methyl omega-hydroxyheptacosanoate is ideal as an internal standard for studies involving long-chain omega-hydroxy fatty acids.1 omega-Hydroxy C27:0 fatty acid and other omega-hydroxy fatty acids can be lactonized by certain enzymes into mono- and oligolactones.2 omega-Oxidation is a minor fatty acid pathway used for fatty acid metabolism and usually occurs in the smooth endoplasmic reticulum. Stimulation of omega-hydroxylation has been proposed as a method for treating X-linked adrenoleukodystrophy, a disease that is characterized by elevated levels of very long chain fatty acids.3 omega-Hydroxy fatty acids have an important role while acylated to various lipids. omega-Hydroxylated very long chain fatty acid (VLCFA) ceramides are vital to skin barrier functions and a deficiency of these lipids can cause death from water loss through the skin. In atopic dermatitis, a common skin disease, there are considerable deficiencies of omegahydroxy long chain fatty acids acylated to ceramides and this may contribute to the severely damaged permeability barrier found in this disease.4
Methyl 30-hydroxytriacontanoate Reference: M1884-25 This product is a high purity omega-hydroxy very long chain fatty acid methyl ester that is ideal as a standard and for biological studies. Omega-oxidation is a minor fatty acid pathway used for fatty acid metabolism and usually occurs in the smooth endoplasmic reticulum. Triacontanoic acid is enzymaticaly converted to the 30-hydroxytriacontanoic acid as well as to the triacontanoyldicarboxylic acid as part of the omega-oxidation metabolic pathway. Stimulation of omega-hydroxylation has been proposed as a method for treating X-linked adrenoleukodystrophy, a disease that is characterized by elevated levels of very long chain fatty acids.1 Omega-hydroxy fatty acids have an important role acylated to various lipids. Omegahydroxylated very long chain fatty acid (VLCFA) ceramides are vital to skin barrier functions and a deficiency of these lipids can cause death from water loss through the skin. A mutation in an elongase enzyme for VLCFA results in a deficiency in omega-hydroxylated VLCFA-ceramides which causes a muscular dystrophy disease, defective skin-water permeability barrier function, and neurological disorders showing the importance of these VLCFA ceramides.2 Sphingolipids (such as sphingomyelin, ceramides, and glucosylceramides) acylated with polyunsaturated and alpha- or omega-hydroxylated VLCFA have been found in the spermatozoa/testes and in the epidermis. Sphingolipids with VLCFA may be responsible for the maturation of these cell.3
N-Tetracosanoyl-sulfatide Reference: M1888-1 Sulfatide is a type of sulfolipid that is found primarily in the central nervous system and is a myelin-specific sphingolipid. A deficiency of sulfatide in white and gray matter has been associated with Alzheimer’s disease and other types of dementia. Apoliprotein E plays an important regulating role in the metabolism of sulfatides.1 A production of anti-sulfatide antibodies in the cerebrospinal fluid, leading to a deficiency in sulfatides, may be a cause of degeneration of the myelin sheath, leading to multiple sclerosis.2 Metachromatic leukodystrophy is an inherited disorder characterized by a deficiency of the lysosomal enzyme arylsulfatase A and the subsequent accumulation of sulfatide in neural and visceral tissues.3 An immunomodulatory role for sulfatides has been suggested in the pathogenesis of tuberculosis. Sulfatides decrease the in vitro production of proinflammatory cytokines. Tetracosanoyl sulfatide is the predominant natural sulfatide species.4
N-Heptadecanoyl-sphingosylphosphorylcholine Reference: M1890-5 This sphingomyelin contains C17:0 which is an unnatural fatty acid making it an ideal internal standard and biological marker.1 The activity of C17 sphingomyelin is very similar to natural sphingomyelin due to their structural similarities.2 Sphingomyelin is found in mammalian cell membranes, especially in the membranes of the myelin sheath. It is the most abundant sphingolipid in mammals and is thought to be found mostly in the exoplasmic leaflet of the membrane although there is also evidence of a sphingomyelin pool in the inner leaflet of the membrane. It is involved in signal transduction and apoptosis. An improper ratio of sphingomyelin to ceramide has been shown to be a factor in Niemann-Pick disease3 and neonatal respiratory distress syndrome.4 However, the ratio of sphingomyelin to ceramide is different for different cell types. Sphingomyelin is an important amphiphilic component when plasma lipoprotein pools expand in response to large lipid loads or metabolic abnormalities.
3-keto-C6-Dihydrosphingosine•HCl Reference: M1891-10 3-keto-Dihydrosphingosine is a vital intermediate in the biosynthesis of ceramides.1,2 This lyso-sphingolipid is formed by the condensation of L-serine and palmitoyl-CoA by the serine palmitoyl transferase enzyme.3 It is then reduced to dihydrosphingosine, converted to ceramide, and eventually synthesized into many types of sphingolipids. C18-ketodihydrosphingosine is the major sphingolipid precursor in the early and intermediate stages of cell life with C20-ketodihydrosphingosine as a minor component. Towards the end of the cell’s life the ratio of C18 to C20 ketodihydrosphingosine becomes more equal. It is a critical regulating step in the availability of sphingolipids in cells. Vitamin K deficiency results in the inactivation of the serine palmitoyl transferase enzyme causing a resultant shortage of sphingolipids. Short-chain analogs of 3-keto-dihydrosphingosine have different physical properties from the long-chain 3- keto-dihydrosphingosines. Short-chain bases are considerably less hydrophobic which could significantly change the process of signal transduction.
3-keto-C8-Dihydrosphingosine•HCl Reference: M1892-10 3-keto-Dihydrosphingosine is a vital intermediate in the biosynthesis of ceramides.1,2 This lyso-sphingolipid is formed by the condensation of L-serine and palmitoyl-CoA by the serine palmitoyl transferase enzyme.3 It is then reduced to dihydrosphingosine, converted to ceramide, and eventually synthesized into many types of sphingolipids. C18-ketodihydrosphingosine is the major sphingolipid precursor in the early and intermediate stages of cell life with C20-ketodihydrosphingosine as a minor component. Towards the end of the cell’s life the ratio of C18 to C20 ketodihydrosphingosine becomes more equal. It seems to be a critical regulating step in the availability of sphingolipids in cells. Vitamin K deficiency results in the inactivation of the serine palmitoyl transferase enzyme causing a resultant shortage of sphingolipids. Short-chain analogs of 3-keto-dihydrosphingosine have different physical properties from the long-chain 3- keto-dihydrosphingosines. Short-chain bases are considerably less hydrophobic which could significantly change the process of signal transduction.
3-keto-C12-Dihydrosphingosine•HCl Reference: M1893-10 3-keto-Dihydrosphingosine is a vital intermediate in the biosynthesis of ceramides.1,2 This lyso-sphingolipid is formed by the condensation of L-serine and palmitoyl-CoA by the serine palmitoyl transferase enzyme.3 It is then reduced to dihydrosphingosine, converted to ceramide, and eventually synthesized into many types of sphingolipids. C18-ketodihydrosphingosine is the major sphingolipid precursor in the early and intermediate stages of cell life with C20-ketodihydrosphingosine as a minor component. Towards the end of the cell’s life the ratio of C18 to C20 ketodihydrosphingosine becomes more equal. It is a critical regulating step in the availability of sphingolipids in cells. Vitamin K deficiency results in the inactivation of the serine palmitoyl transferase enzyme causing a resultant shortage of sphingolipids. Short-chain analogs of 3-keto-dihydrosphingosine have different physical properties from the long-chain 3- keto-dihydrosphingosines. Short-chain bases are considerably less hydrophobic which could significantly change the process of signal transduction.
N-Octanoyl-phytosphingosine Reference: M1894-5 This product is a phytoceramide containing a short chain fatty acid which enables it to more easily enter into cells. Phytosphingosine is a long-chain sphingoid base having important cellular functions such as signaling, cytoskeletal structure, cellular cycle, and heat stress response. It is found largely in mammals, plants, and yeast. Phytosphingosine has seen much use in cosmetics due to its effects on the skin such as reducing inflammation by inhibiting the expression of the allergic cytokines IL-4 and TNF-α and the activation of the transcription factors NF-jB and c-jun in histamine-stimulated skin tissues.1 Phytosphingosine can lead to apoptosis via two distinct pathways and has been investigated as a possible cancer therapeutic treatment. Phytoceramides (fatty acid acylated to Phytosphingosine) are distributed at the microvillous membrane of the epithelial cells of the small intestine. Crypt cells and the adjacent epithelial cells produce phytosphingoglycolipids in much greater quantities than more differentiated epithelial cells.2 The kidney and skin also contain phytosphingoglycolipids although in much lower concentrations than in the small intestine. Phytoceramides form part of the water barrier lipids of the skin. 2-hydroxytetracosanoyl-phytoceramide has recently been shown to have immunostimulating effects in humans.3 Phytoceramides have lately been studied in regards to their role in the central nervous system and have been found to have important functions in neuroprotection.4
N-Hexanoyl-phytosphingosine Reference: M1895-5 This product is a phytoceramide containing a short chain fatty acid, which enables it to more easily enter into cells. Phytosphingosine is a long-chain sphingoid base having important cellular functions such as signaling, cytoskeletal structure, cellular cycle, and heat stress response. It is found largely in mammals, plants, and yeast. Phytosphingosine has seen much use in cosmetics due to its effects on the skin such as reducing inflammation by inhibiting the expression of the allergic cytokines IL-4 and TNF-α and the activation of the transcription factors NF-jB and c-jun in histamine-stimulated skin tissues.1 Phytosphingosine can lead to apoptosis via two distinct pathways and has been investigated as a possible cancer therapeutic treatment. Phytoceramides (fatty acid acylated to Phytosphingosine) are distributed at the microvillous membrane of the epithelial cells of the small intestine. Crypt cells and the adjacent epithelial cells produce phytosphingoglycolipids in much greater quantities than more differentiated epithelial cells.2 The kidney and skin also contain phytosphingoglycolipids although in much lower concentrations than in the small intestine. Phytoceramides form part of the water barrier lipids of the skin. 2-hydroxytetracosanoyl-phytoceramide has recently been shown to have immunostimulating effects in humans.3 Phytoceramides have lately been studied in regards to their role in the central nervous system and have been found to have important functions in neuroprotection.4
N,N-Dihexyl-D-erythro-sphingosine Reference: M1896-1 N,N-Dihexyl-D-erythro-sphingsosine is an unnatural analog of the vital sphingolipid ceramide. Ceramide functions as a precursor in the synthesis of sphingomyelin, complex glycosphingolipids, and free sphingosine and it exerts numerous biological effects, including induction of cell maturation, cell cycle arrest, terminal cell differentiation, cell senescence, and cell death.1 Instead of the normal fatty acid acylated to sphingosine N,N-Dihexyl-D-erythro-sphingsosine contains two hexyl groups making it a tertiary amine rather than secondary. Ceramide analogs, such as N,N-Dihexyl-D-erythro-sphingsosine, are able to induce an a increase in ceramide levels in cells, leading to apoptosis, and may be useful in treating certain diseases.2 N-Hexyl-glucosylceramide is a potent inhibitor of glucosylceramidase, the enzyme responsible for cleaving glucose from glucosylceramide.3