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    Natural Products
    CAS No. 73-03-0 Price $40 / 20mg
    Catalog No.CFN98566Purity>=98%
    Molecular Weight251.24Type of CompoundAlkaloids
    FormulaC10H13N5O3Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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  • Biological Activity
    Description: Cordycepin possesses immunological stimulating,anti-hyperglycemia, anti-cancer, neuroprotective, antifungal, antibacterial, anti-inflammatory, anti-virus and anti-infection activities. Cordycepin has inhibitory effects on osteoclast differentiation in vitro and that it suppresses inflammatory bone loss in vivo. Cordycepin inhibited the production of NO production by down-regulation of iNOS and COX-2 gene expression via the suppression of NF-κB activation, Akt and p38 phosphorylation, suppressed HMGA2, Twist1 and ZEB1-dependent melanoma invasion and metastasis by targeting miR-33b.
    Targets: HMG-CoA Reductase | NF-kB | p38MAPK | TGF-β/Smad | MMP(e.g.TIMP) | NO | NOS | Akt | COX | TNF-α | ERK | JNK | ROS | Calcium Channel | Caspase | Antifection
    In vitro:
    Eur J Pharmacol. 2006 Sep 18;545(2-3):192-9.
    Cordycepin inhibits lipopolysaccharide-induced inflammation by the suppression of NF-kappaB through Akt and p38 inhibition in RAW 264.7 macrophage cells.[Pubmed: 16899239]
    Cordyceps militaris, a caterpillar-grown traditional medicinal mushroom, produces an important bioactive compound, Cordycepin (3'-deoxyadenosine). Cordycepin is reported to possess many pharmacological activities including immunological stimulating, anti-cancer, anti-virus and anti-infection activities. The molecular mechanisms of Cordycepin on pharmacological and biochemical actions of macrophages in inflammation have not been clearly elucidated yet.
    In the present study, we tested the role of Cordycepin on the anti-inflammation cascades in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. In LPS-activated macrophage, nitric oxide (NO) production was inhibited by butanol fraction of C. militaris and the major component of C. militaris butanol faction was identified as Cordycepin by high performance liquid chromatography. To investigate the mechanism by which Cordycepin inhibits NO production and inducible nitric oxide synthase (iNOS) expression, we examined the activation of Akt and MAP kinases in LPS-activated macrophage. Cordycepin markedly inhibited the phosphorylation of Akt and p38 in dose-dependent manners in LPS-activated macrophage. Moreover, Cordycepin suppressed tumor necrosis factor (TNF-alpha) expression, IkappaB alpha phosphorylation, and translocation of nuclear factor-kappaB (NF-kappaB). The expressions of cycloxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were significantly decreased in RAW 264.7 cell by Cordycepin.
    Taken together, these results suggest that Cordycepin inhibits the production of NO production by down-regulation of iNOS and COX-2 gene expression via the suppression of NF-kappaB activation, Akt and p38 phosphorylation. Thus, Cordycepin may provide a potential therapeutic approach for inflammation-associated disorders.
    J Agric Food Chem. 2000 Jul;48(7):2744-8.
    Cordycepin: selective growth inhibitor derived from liquid culture of Cordyceps militaris against Clostridium spp.[Pubmed: 10898616]
    The growth responses of nine human intestinal bacteria to liquid culture of Cordyceps militaris Link. Pt. (Ascomycotina: Clavicipitaceae) collected from a pupa of Bombyx mori L. (Lepidoptera: Bombycidae) were examined using spectrophotometric and impregnated paper disk methods and compared to those of tetracycline and chloramphenicol, as well as those of Coptis japonica root-derived berberine chloride.
    The biologically active constituent of the cultures was characterized as Cordycepin (3'-deoxyadenosine) by spectroscopic analysis. This compound revealed potent growth-inhibiting activity toward Clostridium paraputrificum and Clostridium perfringens at 10 microgram/disk without adverse effects on the growth of Bifidobacterium bifidum, Bifidobacterium breve, Bifidobacterium longum, Bifidobacterium adolescentis, Lactobacillus acidophilus, and Lactobacillus casei, whereas tetracycline and chloramphenicol inhibited the growth of these lactic acid-producing bacteria, clostridia and Escherichia coli. However, C. militaris-derived materials revealed no growth stimulation on the bifidobacteria and lactobacilli.
    These results may be an indication of at least one of the pharmacological actions of C. militaris. As a naturally occurring antibacterial agent, Cordycepin could be useful as a new preventive agent against various diseases caused by clostridia.
    In vivo:
    Nutr Res. 2015 May;35(5):431-9.
    Cordycepin from Cordyceps militaris prevents hyperglycemia in alloxan-induced diabetic mice.[Pubmed: 25940982]
    Cordyceps militaris has long been used in prescriptions of traditional Chinese medicine as a tonic for the treatment of metabolic syndrome. Cordycepin with proven immunomodulatory, antitumor, and hepatoprotective properties is the main active metabolite of C militaris. Diabetes mellitus is a group of metabolic diseases in which the body is unable to regulate blood sugar levels. Hence, we hypothesized that Cordycepin can normalize blood sugar levels and improve the indicators of diabetes.
    The aim of this study was to investigate the possible effects of Cordycepin from C militaris on diabetes in an alloxan-induced diabetic mouse model. Diabetic mice were intraperitoneally administered different doses of Cordycepin (8, 24, and 72 mg/kg body weight) daily for 21 days. Acute toxicity test on normal mice was carried out by giving them maximum tolerance dose of Cordycepin (3600 mg/kg) daily. A 47% reduction of the blood glucose level, 214% increase of hepatic glycogen content, and significant improvement of oral glucose tolerance were noticed after the effective dose of Cordycepin was administered. Polyphagia and polydipsia, the typical symptoms of diabetes, were partly alleviated. Moreover, Cordycepin offered protective effects against diabetes-related kidney and spleen injury. Maximum tolerance dose test indicated that Cordycepin at the large dose of 3600 mg/kg did not show significant effect on body weight and major organ in normal mice after intraperitoneal administration for 14 days.
    The results showed that Cordycepin from C militaris that elicited hypoglycemic activity contributes to the regulation of glucose metabolism in liver in alloxan-induced diabetic mice. Therefore, a Cordycepin treatment during diabetes can improve some of the metabolic syndrome symptoms by regulation of glucose absorption in vivo. Cordycepin may serve as a therapeutic agent in the treatment of diabetes and its related complications.
    Zhongguo Zhong Yao Za Zhi. 2014 Nov;39(21):4096-101.
    Mechanisms of cordycepin on improving renal interstitial fibrosis via regulating eIF2α/TGF-β/Smad signaling pathway[Pubmed: 25775775]
    To investigate the effects and mechanisms of Cordycepin,an effective component of cordyceps militaris, on renal interstitial fibrosis (RIF) and its related eIF2α/TGF-β/Smad signaling pathway.
    Firstly, 15 C57BL/6 mice were randomly divided into 3 groups,the control group (Group A), the model group (Group B) and the Cordycepin-treated group (Group C). After renal interstitial fibrotic model was successfully established by unilateral ureteral obstruction (UUO), the mice in Group C were intraperitoneally administrated with Cordycepin(5 mg x kg(-1) d(-1)) and the ones in Group A and B were administrated with physiological saline for 5 days. At the end of the study, the obstructed kidneys were collected and detected for the pathological changes of RIF, and the mRNA expressions of collagen type I (Col I) and α-smooth muscle actin (α-SMA) in the kidney by Northern blot. Secondly, after renal tubular epithelial (NRK-52E) cells cultured in vitro were exposed to transforming growth factor (TGF) -β with or without Cordycepin, the mRNA expressions of Col I and collagen type IV( Col IV) by Northern blot, and the protein expressions of eukaryotic initiation factor 2α (eIF2α), phosphorylated eIF2α ( p-eIF2α), Smad2/3 and phosphorylated Smad2/3 (p-Smad2/3) were tested by Western blot. In vivo, Cordycepin alleviated RIF in model mice, including improving fibrotic pathological characteristics and mRNA expressions of Col I and α-SMA. In vitro, Cordycepin induced the high expression of p-elF2α, and inhibited the expressions of p-Smad2/3, Col I and Col IV induced by TGF-β in NRK-52E cells.
    Cordycepin attenuates RIF in vivo and in vitro, probably by inducing the phosphorylation of eIF2α, suppressing the expression of p-Smad2/3, a key signaling molecule in TGF-β/Smad signaling pathway, and reducing the expressions of collagens and α-SMA in the kidney.
    Eur J Pharmacol. 2011 Aug 16;664(1-3):20-8.
    Cordycepin protects against cerebral ischemia/reperfusion injury in vivo and in vitro.[Pubmed: 21554870 ]
    Cordycepin, (3'-deoxyadenosine), a bioactive compound of Cordyceps militaris, has been shown to exhibit many pharmacological actions, such as anti-inflammatory, antioxidative and anticancer activities. Little is known about the neuroprotective action of Cordycepin as well as its molecular mechanisms.
    In this study, Cordycepin was investigated for its neuroprotective potential in mice with ischemia following 15 min of the bilateral common carotid artery occlusion and 4h of reperfusion. The effect of Cordycepin was also studied in mice brain slices treated with oxygen-glucose deprivation (OGD) injury. Our results showed that Cordycepin was able to prevent postischemic neuronal degeneration and brain slice injury. Excitatory amino acids such as glutamate and aspartate in brain homogenized supernatant, which were increased in ischemia/reperfusion group, were detected by high performance liquid chromatography (HPLC). The results showed that Cordycepin was able to decrease the extracellular level of glutamate and aspartate significantly. Moreover, Cordycepin was able to increase the activity of superoxide dismutase (SOD) and decrease the level of malondialdehyde (MDA), ameliorating the extent of oxidation. Furthermore, matrix metalloproteinase-3(MMP-3), a key enzyme involved in inflammatory reactions, was markedly increased after ischemia reperfusion, whereas Cordycepin was able to inhibit its expression obviously.
    In conclusion, our in vivo and in vitro study showed that Cordycepin was able to exert a potent neuroprotective function after cerebral ischemia/reperfusion.
    Cordycepin Description
    Source: The body of Cordyceps sienesis (Berkeley) Saccardo
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to:

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.9803 mL 19.9013 mL 39.8026 mL 79.6052 mL 99.5064 mL
    5 mM 0.7961 mL 3.9803 mL 7.9605 mL 15.921 mL 19.9013 mL
    10 mM 0.398 mL 1.9901 mL 3.9803 mL 7.9605 mL 9.9506 mL
    50 mM 0.0796 mL 0.398 mL 0.7961 mL 1.5921 mL 1.9901 mL
    100 mM 0.0398 mL 0.199 mL 0.398 mL 0.7961 mL 0.9951 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Cell Research:
    Oncotarget. 2015 Apr 30;6(12):9834-53.
    Cordycepin (3'-deoxyadenosine) suppressed HMGA2, Twist1 and ZEB1-dependent melanoma invasion and metastasis by targeting miR-33b.[Pubmed: 25868853]
    Malignant melanoma, the most deadly form of skin cancer, has a high propensity for metastatic spread and is notoriously chemotherapy-resistant. Cordycepin, the active component of Cordyceps spp., has been identified to have anti-metastatic effect on tumor progression and thus possesses pharmacological and therapeutic potentials. However, the mechanisms of anti-metastatic effects of Cordycepin at cellular levels remain elusive.
    We analyzed the effect of Cordycepin on human melanoma miRNA expression profiles by miRNAarray and found that miR-33b was upregulated in highly-metastatic melanoma cell lines following Cordycepin exposure. Cordycepin-mediated miR-33b expression was dependent on LXR-RXR heterodimer activation. miR-33b directly binds to HMGA2, Twist1 and ZEB1 3'-UTR to suppress their expression. The negative correlations between miR-33b levels and HMGA2, Twist1 or ZEB1 expression were detected in 72 patient melanoma tissue samples. By targeting HMGA2 and Twist1, miR-33b attenuated melanoma migration and invasiveness upon Cordycepin exposure. miR-33b knockdown or ZEB1 overexpression reverted Cordycepin-mediated mesenchymal-epithelial transition (MET), triggering the expression of N-cadherin. In spontaneous metastasis models, Cordycepin suppressed tumor metastasis without altering primary tumor growth.
    We showed for the first time that targeting miRNA by Cordycepin indicates a new mechanism of Cordycepin-induced suppression of tumor metastasis and miR-33b/HMGA2/Twist1/ZEB1 axis plays critical roles in regulating melanoma dissemination.
    Neurotoxicology. 2014 Mar;41:102-11.
    The neuroprotective effects of cordycepin inhibit glutamate-induced oxidative and ER stress-associated apoptosis in hippocampal HT22 cells.[Pubmed: 24486958 ]
    Glutamate toxicity increases the formation of reactive oxygen species (ROS) and intracellular calcium levels, resulting in neuronal dysfunction, neurodegenerative disorders, and death. Cordycepin is a derivative of the nucleoside adenosine, and is believed to exert neuroprotective effects against glutamate-induced oxidative toxicity in HT22 neuronal cells.
    Excessive glutamate induces oxidative and endoplasmic reticulum (ER) stress, gradually increasing ER-related pro-apoptotic transcription factor C/EBP homologous protein (CHOP) expression, and eventually up-regulating expression of the pro-apoptotic factor Bax. Cordycepin inhibits CHOP and Bax expressions, as well as p-ERK, p-JNK, and p-p38, all of which are involved in oxidative or ER stress-induced apoptosis. In addition, the increased production of ROS from excessive glutamate leads to elevation of mitochondrial membrane potential (MMP), a hallmark of mitochondrial dysfunction. Cordycepin retains MMP and reduces the elevated levels of ROS and Ca(2+) induced by glutamate. Caspases are crucial mediators involved in mitochondrial apoptosis, and while glutamate disrupts mitochondrial function, it does not change expression levels of caspase 3 and caspase 9. Similarly, Cordycepin has no effect on caspase 3 and caspase 9 expressions; however, it decreases the expression of ER stress-specific caspase 12, which plays a key role in the initiation of ER stress-induced apoptosis. Finally, we found that the anti-apoptotic effects of Cordycepin are partially dependent on activation of the adenosine A1 receptor, whereas an antagonist selectively attenuated the neuroprotective effects of Cordycepin.
    Collectively, these results suggest that Cordycepin could be a potential future therapeutic agent for neuronal disorders.
    Animal Research:
    J Med Food. 2015 Apr;18(4):446-52.
    Cordyceps militaris mushroom and cordycepin inhibit RANKL-induced osteoclast differentiation.[Pubmed: 25789604 ]
    Cordyceps militaris is a medicinal mushroom and its bioactive compound, Cordycepin, is reported to have many pharmacological activities. The goal of this study was to investigate the effects of C. militaris extract (CME) and Cordycepin on osteoclast differentiation in vitro and on an inflammatory bone loss in vivo.
    In RAW 264.7 cells, CME and Cordycepin showed dose-dependent inhibition of receptor activator of the nuclear factor kappa B (NF-κB) ligand (RANKL)-induced osteoclast differentiation by TRAP (tartrate-resistant acid phosphatase) staining. Moreover, the mRNA expression of osteoclastogenesis-related genes (TRAP, cathepsin K, MMP-9, and NFATc1) was also inhibited by CME and Cordycepin. Also, Cordycepin significantly inhibited RANKL-induced phosphorylation of p38 and NF-κB, but not that of other members of mitogen-activated protein kinase families. To examine the effect of CME on bone loss in vivo, we used a mouse model of lipopolysaccharide (LPS)-mediated bone loss. Micro-CT analysis of the femurs showed that LPS treatment caused bone loss. However, bone loss was significantly attenuated in mice treated with CME.
    These results suggest that Cordycepin or/and CME have inhibitory effects on osteoclast differentiation in vitro and that they suppress inflammatory bone loss in vivo.
    Antimicrob Agents Chemother. 1998 Jun;42(6):1424-7.
    Antifungal activity of 3'-deoxyadenosine (cordycepin).[Pubmed: 9624488]
    The antifungal activity of the nucleoside analog 3'-deoxyadenosine (Cordycepin) was studied in a murine model of invasive candidiasis.
    When protected from deamination by either deoxycoformycin or coformycin, both of which are adenosine deaminase inhibitors, Cordycepin exhibited potent antifungal efficacy, as demonstrated by prolongation of survival and a decrease in CFU in the kidneys of mice treated with Cordycepin plus an adenosine deaminase inhibitor. The antifungal effect was seen with three different Candida isolates: Candida albicans 64, a relatively fluconazole-resistant clinical isolate of C. albicans (MIC, 16 micrograms/ml), and the fluconazole-resistant Candida krusei.
    Cordycepin and related compounds may provide another avenue for the discovery of clinically useful antifungal drugs.