Shipping to Germany We Offer Worldwide Shipping
Login Wishlist

Cordycepin

$85

  • Brand : BIOFRON

  • Catalogue Number : BF-C1015

  • Specification : 98%

  • CAS number : 73-03-0

  • Formula : C10H13N5O3

  • Molecular Weight : 251.24

  • PUBCHEM ID : 6303

  • Volume : 20mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-C1015

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

251.24

Appearance

White crystalline powder

Botanical Source

Cordyceps militaris

Structure Type

Nucleosiede

Category

Standards;Natural Pytochemical;API

SMILES

C1C(OC(C1O)N2C=NC3=C(N=CN=C32)N)CO

Synonyms

9H-Purin-6-amine, 9-(3-deoxy-β-D-erythro-pentofuranosyl)-/Adenine cordyceposide/9H-Purine, 6-amino-9-(3-deoxy-β-D-ribofuranosyl)-/Adenosine,3-deoxy/Cordycepine/Cordycepin/Cordyceps fungus powder/cordycepin crystalline/3'-Deoxyadenosine/adenosine, 3'-deoxy-/(-)-cordycepin/3'-Deoxy-D-adenosine

IUPAC Name

(2R,3R,5S)-2-(6-aminopurin-9-yl)-5-(hydroxymethyl)oxolan-3-ol

Applications

Cordycepin, which is a nucleoside derivative isolated from Cordyceps, inhibits IL-1β-induced MMP-1 and MMP-3 expression in rheumatoid arthritis synovial fibroblasts (RASFs) in a dose-dependent manner.

Density

1.9±0.1 g/cm3

Solubility

Methanol; Water; DMSO

Flash Point

333.1±34.3 °C

Boiling Point

627.2±65.0 °C at 760 mmHg

Melting Point

225-229ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2934990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:73-03-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30287757

Abstract

Cordyceps is a genus of ascomycete fungi that has been used for traditional herbal remedies. It contains various bioactive ingredients including cordycepin. Cordycepin, also known as 3-deoxyadenosine, is a major compound and has been suggested to have anticancer potential. The treatment of various cancer cells with cordycepin in effectively induces cell death and retards their cancerous properties. However, the underlying mechanism is not fully understood. Recent evidence has shed light on the molecular pathways involving cysteine-aspartic proteases (caspases), mitogen-activated protein kinases (MAPKs), and glycogen synthase kinase 3 beta (GSK-3β). Furthermore, the pathways are mediated by putative receptors, such as adenosine receptors (ADORAs), death receptors (DRs), and the epidermal growth factor receptor (EGFR). This review provides the molecular mechanisms by which cordycepin functions as a singular or combinational anticancer therapeutic agent.

KEYWORDS

Cordyceps; adenosine receptors; anticancer; cordycepin; death receptors

Title

The Anticancer Properties of Cordycepin and Their Underlying Mechanisms.

Author

Yoon SY1, Park SJ2, Park YJ3.

Publish date

2018 Oct 4

PMID

29054740

Abstract

Acute lung injury (ALI) is a common severe clinical syndrome in intensive care unit. Inflammation has been reported to play a critical role in the development of ALI. Cordycepin, an active component isolated from Cordyceps militaris, has been reported to have anti-inflammatory effects. However, the anti-inflammatory effects of cordycepin on LPS-induced ALI remain unclear. Therefore, in the present study, we assessed whether cordycepin could attenuate ALI induced by LPS. The mice were conditioned with cordycepin 1h before intranasal instillation of LPS. Lung wet/dry (W/D) ratio, MPO activity, MDA content, and inflammatory cytokines production were detected. The expression of NF-κB p65, I-κB, Nrf2, and HO-1 were detected by western blot analysis. We found that LPS significantly increased lung wet/dry (W/D) ratio, MPO activity, MDA content, and inflammatory cytokines production. However, the increases were significantly inhibited by treatment of cordycepin. LPS-induced NF-κB activation was also suppressed by cordycepin. In addition, cordycepin was found to up-regulate the expression of Nrf2 and HO-1 in a dose-dependent manner. In conclusion, our results demonstrated that cordycepin could attenuate LPS-induced ALI effectively, probably due to inhibition of inflammation and oxidative stress.

Copyright © 2017 Elsevier B.V. All rights reserved.

KEYWORDS

Cordycepin; LPS; Lung injury; NF-κB; Nrf2

Title

Cordycepin inhibits LPS-induced acute lung injury by inhibiting inflammation and oxidative stress.

Author

Lei J1, Wei Y1, Song P1, Li Y1, Zhang T1, Feng Q2, Xu G3.

Publish date

2018 Jan 5

PMID

32268154

Abstract

Acute pancreatitis (AP) is a noninfectious inflammatory disease with high morbidity and mortality, which is characterized by severe inflammation and tissue necrosis. Cordycepin (CRD), derived from Cordyceps militaris, possesses anti-inflammatory effects and immunomodulation properties. Here, we investigated the protective effects of CRD on pancreatic injury and clarified potential mechanisms in AP model. There were established caerulein-induced AP and CRD pretreatment models in vivo and in vitro, as showed by serum enzymes, histopathological alterations and pro-inflammatory cytokines. Pretreatment with CRD notably downregulated the serum amylase and lipase levels and apparently reduced pancreatic histopathological alterations in AP mice. Meanwhile, the MPO staining confirmed that CRD pretreatment modulated the infiltration of neutrophils in AP mice. Furthermore, CRD markedly decreased the levels of pro-inflammatory factors (IL-6, IL-1β, and TNF-α) though inhibiting the activation of nuclear factor-κB (NF-κB) and NLR family pyrin domain-containing protein 3 (NLRP3) inflammasome in AP mice. In pancreatic acinar cancer cell 266-6, CRD pretreatment decreased cholecystokinin(CCK)-induced inflammatory response was consistent with those in vivo. Mechanistically, CRD was also revealed to activate activated protein kinase (AMPK) and attenuated inflammation both in vivo and in vitro. On the whole, this study indicated that CRD protects mice from pancreatic inflammatory process and damage by suppressed NF-κB and NLRP3 inflammasome activation via AMPK, which probably contributed to the potential therapy for AP.

Copyright © 2020. Published by Elsevier Inc.

KEYWORDS

AMPK; Acute pancreatitis; Cordycepin; Inflammation; NF-κB/NLRP3

Title

Cordycepin protects against acute pancreatitis by modulating NF-κB and NLRP3 inflammasome activation via AMPK.

Author

Yang J1, Zhou Y2, Shi J3.

Publish date

2020 Apr 5