D-erythro Lysosphingomyelin (d18:1) - CAS:1670-26-4

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D-erythro Lysosphingomyelin (d18:1) (Synonyms:鞘氨醇磷酸胆碱；Sphingosylphosphorylcholine)

目录号 : KCM11899 CAS No. : 1670-26-4 纯度 : ≥98%

Data Sheet 产品使用指南

D-erythro Lysosphingomyelin is a bioactive sphingolipid. It is an agonist of sphingosine-1-phosphate receptor 1 (S1P), S1P, and S1P (ECs = 167.7, 368.1, and 482.6 nM, respectively, for the human receptors). D-erythro Lysosphingomyelin is also an agonist of the orphan receptor ovarian cancer G protein-coupled receptor 1 (ORG1) that induces calcium accumulation in cells overexpressing OGR1 (EC = ~35 nM). Levels of D-erythro lysosphingomyelin are increased in skin isolated from patients with atopic dermatitis, as well as postmortem brain from patients with Niemann-Pick disease type A, but not type B. As this product is derived from a natural source, there may be variations in the sphingoid backbone.

规格	价格	是否有货
1mg		In-stock
5mg		In-stock
10mg	询价	In-stock
25mg	询价	In-stock

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生物活性

D-erythro Lysosphingomyelin (d18:1) is a bioactive lipid and a major component of plasma high-density lipoprotein that binds to OGR1 with a Kd of 33.3 nM. D-erythro Lysosphingomyelin (d18:1) triggers delayed phosphorylation of Smad2, upregulates α-SMA expression, and activates TRPM3. D-erythro Lysosphingomyelin (d18:1) reduces Apoptosis and upregulates the expression of uPA and its receptor uPA-R. D-erythro Lysosphingomyelin (d18:1) exerts anti-apoptotic, anti-cardiac hypertrophy and pro-wound healing effects. D-erythro Lysosphingomyelin (d18:1) induces scratching behavior in mice. D-erythro Lysosphingomyelin (d18:1) is used in studies related to atopic dermatitis, promyelocytic leukemia, heart failure, myocardial ischemia/reperfusion injury, ovarian cancer, breast cancer, pancreatic cancer, and skin wound healing disorders in genetically impaired healing diabetes

体外研究

D-erythrolysphingomyelin (d18:1) (10 nM-50 μM) activates TRPM3 in a dose-dependent manner, inducing extracellular calcium influx and mobilizing intracellular calcium stores in HEK293T cells.
D-erythrolysphingomyelin (d18:1) (15-20 μM; 15 min-4 h) can effectively induce actin stress fiber formation and adhesive patch assembly in mouse embryonic stem cell-derived embryoid like growth products in a concentration - and time-dependent manner.
D-erythrolysphingomyelin (d18:1) (10 μM) can inhibit angiotensin II induced hypertrophy of neonatal mouse cardiomyocytes.
D-erythrolysphingomyelin (d18:1) (10 μM) can protect neonatal rat cardiomyocytes from apoptosis induced by 210 min hypoxia followed by 150 min reoxygenation.
D-erythrolysphingomyelin (d18:1) can bind to OGR1 in HEK293 cells transfected with OGR1 with high affinity (Kd=33.3 nM) and high specificity.
D-erythrolysphingomyelin (d18:1) (0.1-5 μM; 24 h) can upregulate the expression of urokinase type plasminogen activator (uPA) and its receptor uPA-R on the surface of normal foreskin keratinocytes in a dose-dependent manner within 24 h.

Cell Proliferation Assay

Cell Line:

human NB4 promyelocytic leukemia cells

Concentration:

12.5-15 μM

Incubation Time:

48-96 hours

Result:

Caused a 45% decrease in NB4 cell numbers after 96 h compared to untreated controls.
Significantly increased relative CD11c mRNA expression at 48 h and 96 h, reaching ~10% of the effect of all-trans retinoic acid (ATRA).
Significantly increased relative CD18 mRNA expression at 48 h and 96 h, reaching 8-18% of the effect of ATRA.
Substantially increased cell surface CD11c protein expression, reaching ~20% of the effect of ATRA.

体内研究

D-erythrolysphingomyelin (d18:1) (100 nmol per site; Intradermal injection can induce significant scratching behavior in Mus musculus, but does not induce pain related wiping behavior, confirming its itch inducing activity.
D-erythrolysphingomyelin (d18:1) (10 μM/kg/day; Subcutaneous injection; Daily; Lasting for 4 weeks, it can increase the survival rate of mice to 63% and alleviate pressure overload induced myocardial hypertrophy, fibrosis, and cell apoptosis by inhibiting the CaM-JNK/p38 signaling pathway.
D-erythrolysphingomyelin (d18:1) (0.625-2.5 μg/g body weight; intravenous injection; Prophylactic treatment 30 minutes before coronary artery ligation or treatment at the beginning of reperfusion can dose dependently reduce myocardial infarction area through a mechanism dependent on S1P3 receptors: the reduction can reach 50% during prophylactic treatment and 40% during reperfusion.
D-erythro Lysosphingomyelin (d18:1) (2 μM; local) can statistically significantly promote skin wound healing in diabetes db/db mice with impaired healing ability at the gene level, which is manifested by the reduction of wound area, the increase of granulation tissue volume, and the shortening of non epithelialized wound length.

Animal Model:	C57BL/6 (male, 10- to 14-week-old)
Dosage:	100 nmol/site
Administration:	i.d.; single administration
Result:	Induced a mean of 74.83 ± 27.46 scratching bouts per 30 min, compared to 12 ± 4.374 scratching bouts in vehicle-treated mice. Did not induce a significant change in wiping behavior, with a mean of 4.000 ± 0.578 wiping bouts per 30 min, compared to 6.333 ± 0.989 in vehicle-treated mice.\nInduced a mean of 89.67 ± 7.756 scratching bouts per 30 min, compared to 14.33 ± 3.303 scratching bouts in vehicle-treated mice.

Animal Model:	C57BL/6 (male, 6-8 weeks old; pressure overload induced via trans-aortic constriction surgery)
Dosage:	10 μM/kg/day
Administration:	s.c.; daily; 4 weeks
Result:	Increased survival rate to 63% in TAC mice. Significantly increased left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) relative to untreated TAC mice. Significantly reduced the ratios of heart weight to body weight (HW/BW) and left ventricular weight to body weight (LW/BW) relative to untreated TAC mice. Reduced cardiomyocyte cross-sectional area relative to untreated TAC mice. Decreased the mRNA and protein expression of hypertrophy markers ANP, BNP, and β-MHC compared to untreated TAC mice. Reduced left ventricular collagen volume fraction relative to untreated TAC mice. Decreased protein and mRNA expression of fibrosis markers collagen I, collagen III, α-SMA, TGF-β, and fibronectin relative to untreated TAC mice. Reduced the number of TUNEL-positive apoptotic cardiomyocytes relative to untreated TAC mice. Decreased protein expression of Bax in TAC mouse hearts compared to untreated TAC mice. Increased protein expression of Bcl-2 in TAC mouse hearts compared to untreated TAC mice. Reduced the levels of CaM, phosphorylated JNK (p-JNK), and phosphorylated p38 (p-p38) in TAC mouse hearts compared to untreated TAC mice.

Animal Model:	Outbred Swiss mice (strain-matched, age-matched, sex-matched); C57BL/6 wild-type mice; S1P₃-deficient (S1P₃^-/^-) mice on C57BL/6 background (strain-matched, age-matched, sex-matched)
Dosage:	0.625 μg/g body weight; 1.25 μg/g body weight; 2.5 μg/g body weight
Administration:	i.v.; 30 minutes before coronary ligation; single dose; i.v. (therapeutically at reperfusion onset; single dose)
Result:	Reduced infarct size by 23% (0.625 μg/g preventive). Reduced infarct size by 36% (1.25 μg/g preventive). Reduced infarct size by 50% (2.5 μg/g preventive). Reduced infarct size by 40% (1.25 μg/g at reperfusion). Reduced polymorphonuclear neutrophil recruitment to infarcted area from 629 ± 45 PMN/mm² to 332 ± 43 PMN/mm² (preventive treatment). Reduced TUNEL-positive apoptotic cells in area at risk from 920 ± 225 cells/mm² to 643 ± 66 cells/mm² (preventive treatment). Reduced infarction/area at risk to 29 ± 3.8% vs control 34 ± 2% (1.25 μg/g preventive in C57BL/6 wild-type mice). Showed no effect on infarct size (105 ± 9% of vehicle control, no significant difference) in S1P₃^-/^- mice.

分子式

C₂₃H₄₉N₂O₅P

分子量

464.62

CAS号

1670-26-4

中文名称

溶血神经鞘磷脂；(S)-(对甲苯亚砜基)二茂铁;4-异丙氧基苯酚;溶血神经鞘磷脂;D-赤藓-鞘氨醇磷酸胆碱

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

-20°C, protect from light, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)

溶解性数据

In Vitro:

Ethanol : 2.5 mg/mL (5.38 mM; ultrasonic and warming and heat to 60°C)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	2.1523 mL	10.7615 mL	21.5230 mL
5 mM	0.4305 mL	2.1523 mL	4.3046mL
10 mM	---	---	---

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

纯度： ≥98%