Shipping to United States We Offer Worldwide Shipping
Login Wishlist

Sipeimine-3β-D-glucoside

$300

  • Brand : BIOFRON

  • Catalogue Number : AV-H24046

  • Specification : 98%

  • CAS number : 32685-93-1

  • Formula : C33H53NO8

  • Molecular Weight : 591.77

  • PUBCHEM ID : 90479257

  • Volume : 20mg

Available on backorder

Quantity
Checkout Bulk Order?

Catalogue Number

AV-H24046

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

591.77

Appearance

Powder

Botanical Source

Fritillaria walujewii Regel; Fritillaria pallidiflora Schrenk/ Alkaloid from Petilium eduardii (Liliaceae)

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

CC1CCC2C(C3CCC4C(C3CN2C1)CC5C4CC(=O)C6C5(CCC(C6)OC7C(C(C(C(O7)CO)O)O)O)C)(C)O

Synonyms

(3β,5α)-20-Hydroxy-6-oxocevan-3-yl β-D-glucopyranoside/SipeiMine-3Beta-D-glucoside/Cevan-6-one, 3-(β-D-glucopyranosyloxy)-20-hydroxy-, (3β,5α)-/Edpetiline

IUPAC Name

(1R,2S,6S,9S,10S,11S,14S,15S,18S,20S,23R,24S)-10-hydroxy-6,10,23-trimethyl-20-[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-4-azahexacyclo[12.11.0.02,11.04,9.015,24.018,23]pentacosan-17-one

Applications

Edpetiline is a principal alkaloid from P. eduardi. Edpetiline has significant antiinflammatory effects[1].

Density

1.3±0.1 g/cm3

Solubility

Methanol; Water

Flash Point

403.0±32.9 °C

Boiling Point

742.7±60.0 °C at 760 mmHg

Melting Point

272-276℃ (methanol )

InChl

InChI=1S/C33H53NO8/c1-16-4-7-27-33(3,40)22-6-5-18-19(21(22)14-34(27)13-16)11-23-20(18)12-25(36)24-10-17(8-9-32(23,24)2)41-31-30(39)29(38)28(37)26(15-35)42-31/h16-24,26-31,35,37-40H,4-15H2,1-3H3/t16-,17-,18+,19+,20-,21-,22-,23-,24+,26+,27-,28+,29-,30+,31+,32+,33-/m0/s1

InChl Key

DHQFYEJMFMYGCV-RRIRULBESA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:32685-93-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

24089517

Abstract

Endocannabinoid signaling has been implicated in modulating insulin release from β cells of the endocrine pancreas. β Cells express CB1 cannabinoid receptors (CB1Rs), and the enzymatic machinery regulating anandamide and 2-arachidonoylglycerol bioavailability. However, the molecular cascade coupling agonist-induced cannabinoid receptor activation to insulin release remains unknown. By combining molecular pharmacology and genetic tools in INS-1E cells and in vivo, we show that CB1R activation by endocannabinoids (anandamide and 2-arachidonoylglycerol) or synthetic agonists acutely or after prolonged exposure induces insulin hypersecretion. In doing so, CB1Rs recruit Akt/PKB and extracellular signal-regulated kinases 1/2 to phosphorylate focal adhesion kinase (FAK). FAK activation induces the formation of focal adhesion plaques, multimolecular platforms for second-phase insulin release. Inhibition of endocannabinoid synthesis or FAK activity precluded insulin release. We conclude that FAK downstream from CB1Rs mediates endocannabinoid-induced insulin release by allowing cytoskeletal reorganization that is required for the exocytosis of secretory vesicles. These findings suggest a mechanistic link between increased circulating and tissue endocannabinoid levels and hyperinsulinemia in type 2 diabetes.

KEYWORDS

Cannabinoid Receptors, Cytoskeleton, Endocannabinoids, Exocytosis, Focal Adhesion Kinase, Insulin Release

Title

CB1 Cannabinoid Receptors Couple to Focal Adhesion Kinase to Control Insulin Release*

Author

Katarzyna Malenczyk,‡§,1 Magdalena Jazurek,‡,2 Erik Keimpema,§,2 Cristoforo Silvestri,¶ Justyna Janikiewicz,‡ Ken Mackie,? Vincenzo Di Marzo,¶ Maria J. Redowicz,‡ Tibor Harkany,§**,3 and Agnieszka Dobrzyn‡,4

Publish date

2013 Oct 2

PMID

2690996

Title

The clinical immunobiology of interleukin-2: potential modified uses for improved cancer treatment.

Author

S. D. Voss, G. Weil-Hillman, J. A. Hank, J. A. Sosman, and P. M. Sondel

Publish date

1989 Jan

PMID

8643678

Abstract

Recombination repair protein 1 (Rrp1) includes a C-terminal region homologous to several DNA repair proteins, including Escherichia coli exonuclease III and human APE, that repair oxidative and alkylation damage to DNA. The nuclease activities of Rrp1 include apurinic/apyrimidinic endonuclease, 3′-phosphodiesterase, 3′-phosphatase, and 3′-exonuclease. As shown previously, the C-terminal nuclease region of Rrp1 is sufficient to repair oxidative- and alkylation-induced DNA damage in repair-deficient E. coli mutants. DNA strand-transfer and single-stranded DNA renaturation activities are associated with the unique N-terminal region of Rrp1, which suggests possible additional functions that include recombinational repair or homologous recombination. By using the Drosophila w/w+ mosaic eye system, which detects loss of heterozygosity as changes in eye pigmentation, somatic mutation and recombination frequencies were determined in transgenic flies overexpressing wild-type Rrp1 protein from a heat-shock-inducible transgene. A large decrease in mosaic clone frequency is observed when Rrp1 overexpression precedes treatment with gamma-rays, bleomycin, or paraquat. In contrast, Rrp1 overexpression does not alter the spot frequency after treatment with the alkylating agents methyl methanesulfonate or methyl nitrosourea. A reduction in mosaic clone frequency depends on the expression of the Rrp1 transgene and on the nature of the induced DNA damage. These data suggest a lesion-specific involvement of Rrp1 in the repair of oxidative DNA damage.

Title

Overexpression of a Rrp1 transgene reduces the somatic mutation and recombination frequency induced by oxidative DNA damage in Drosophila melanogaster.

Author

A Szakmary, S M Huang, D T Chang, P A Beachy, and M Sander

Publish date

1996 Feb 20