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Inosine

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-I2008

  • Specification : 98%

  • CAS number : 58-63-9

  • Formula : C10H12N4O5

  • Molecular Weight : 268.23

  • PUBCHEM ID : 135398641

  • Volume : 20mg

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Catalogue Number

BF-I2008

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

268.23

Appearance

White powder

Botanical Source

Cordyceps sinensis

Structure Type

Nucleosiede

Category

Standards;Natural Pytochemical;API

SMILES

C1=NC2=C(C(=O)N1)N=CN2C3C(C(C(O3)CO)O)O

Synonyms

6-Oxopurine riboside/HXR/RIBOXINE/nosine/Ino/9-β-δ-Ribofuranosylhypoxanthine/Hypoxanthine, 9-β-D-ribofuranosyl-/1,9-dihydro-9-b-D-ribofuranosyl-6H-Purin-6-one/9-β-D-ribofuranosyl-Hypoxanthine/9-β-D-Ribofuranosylhypoxanthine/Inosie/9-[(2R,3R,4S,5R)-3,4-Dihydroxy-5-(hydroxymethyl)tetrahydro-2-furanyl]-1,9-dihydro-6H-purin-6-one/INO 495/hypoxanthine/Oxiamin/9-b-D-Ribofuranosylhypoxanthine/Atorel/6H-Purin-6-one, 1,9-dihydro-9-β-D-ribofuranosyl-/9β-D-Ribofuranosylhypoxanthine/6-oxy-purine riboside/9H-Purin-6-ol, 9-β-D-ribofuranosyl-/9-β-D-ribofuranosyl-1,9-dihydro-6H-purin-6-one/9-b-D-ribofuranosyl-Hypoxanthine/Inosine/9-[(2R,3R,4S,5R)-3,4-Dihydroxy-5-(hydroxymethyl)tetrahydro-2-furanyl]-1,9-dihydro-6H-purin-6-one/T56 BN DN FN HNJ IQ D- BT5OTJ CQ DQ E1Q &&β-D-Ribo Form/Inosine (8CI,9CI)/Selfer

IUPAC Name

9-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1H-purin-6-one

Density

2.1±0.1 g/cm3

Solubility

Methanol; Water; DMSO

Flash Point

359.3±34.3 °C

Boiling Point

670.5±65.0 °C at 760 mmHg

Melting Point

222-226 °C (dec.)(lit.)

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#:58-63-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30509978

Abstract

The emergence of primordial RNA-based life would have required the abiotic synthesis of nucleotides, and their participation in nonenzymatic RNA replication. Although considerable progress has been made toward potentially prebiotic syntheses of the pyrimidine nucleotides (C and U) and their 2-thio variants, efficient routes to the canonical purine nucleotides (A and G) remain elusive. Reported syntheses are low yielding and generate a large number of undesired side products. Recently, a potentially prebiotic pathway to 8-oxo-adenosine and 8-oxo-inosine has been demonstrated, raising the question of the suitability of the 8-oxo-purines as substrates for prebiotic RNA replication. Here we show that the 8-oxo-purine nucleotides are poor substrates for nonenzymatic RNA primer extension, both as activated monomers and when present in the template strand; their presence at the end of a primer also strongly reduces the rate and fidelity of primer extension. To provide a proper comparison with 8-oxo-inosine, we also examined primer extension reactions with inosine, and found that inosine exhibits surprisingly rapid and accurate nonenzymatic RNA copying. We propose that inosine, which can be derived from adenosine by deamination, could have acted as a surrogate for G in the earliest stages of the emergence of life.

Copyright © 2018 the Author(s). Published by PNAS.

KEYWORDS

RNA replication; origin of life; primordial RNA

Title

Inosine, but none of the 8-oxo-purines, is a plausible component of a primordial version of RNA.

Author

Kim SC1, O'Flaherty DK2,3,4, Zhou L2,3,4, Lelyveld VS2,3,4, Szostak JW5,2,3,4.

Publish date

2018 Dec 26

PMID

32156055

Abstract

Human subcutaneous fibroblasts (HSCF) challenged with inflammatory mediators release huge amounts of ATP, which rapidly generates adenosine. Given the nucleoside’s putative relevance in wound healing, dermal fibrosis, and myofascial pain, we investigated the role of its precursor, AMP, and of its metabolite, inosine, in HSCF cells growth and collagen production. AMP (30 µM) was rapidly (t½ 3 ± 1 min) dephosphorylated into adenosine by CD73/ecto-5′-nucleotidase. Adenosine accumulation (t½ 158 ± 17 min) in the extracellular fluid reflected very low cellular adenosine deaminase (ADA) activity. HSCF stained positively against A2A and A3 receptors but were A1 and A2B negative. AMP and the A2A receptor agonist, CGS21680C, increased collagen production without affecting cells growth. The A2A receptor antagonist, SCH442416, prevented the effects of AMP and CGS21680C. Inosine and the A3 receptor agonist, 2Cl-IB-MECA, decreased HSCF growth and collagen production in a MRS1191-sensitive manner, implicating the A3 receptor in the anti-proliferative action of inosine. Incubation with ADA reproduced the inosine effect. In conclusion, adenosine originated from extracellular ATP hydrolysis favors normal collagen production by HSCF via A2A receptors. Inhibition of unpredicted inosine formation by third party ADA cell providers (e.g., inflammatory cells) may be a novel therapeutic target to prevent inappropriate dermal remodeling via A3 receptors activation.

KEYWORDS

adenosine A2A receptor; adenosine A3 receptor; cells proliferation; collagen production; exchange protein activated by cyclic AMP (EPAC) pathway; human subcutaneous fibroblasts; inosine

Title

Opposing Effects of Adenosine and Inosine in Human Subcutaneous Fibroblasts May Be Regulated by Third Party ADA Cell Providers.

Author

Herman-de-Sousa C1, Pinheiro AR1,2, Paramos-de-Carvalho D1, Costa MA1,3, Ferreirinha F1, Magalhães-Cardoso T1, Ribeiro S4, Pelletier J5, Sevigny J5,6, Correia-de-Sa P1.

Publish date

2020 Mar 7

PMID

32045593

Abstract

Bipolar Disorder is a disorder characterized by alternating episodes of depression, mania or hypomania, or even mixed episodes. The treatment consists on the use of mood stabilizers, which imply serious adverse effects. Therefore, it is necessary to identify new therapeutic targets to prevent or avoid new episodes. Evidence shows that individuals in manic episodes present a purinergic system dysfunction. In this scenario, inosine is a purine nucleoside known to act as an agonist of A1 and A2A adenosine receptors. Thus, we aimed to elucidate the preventive effect of inosine on locomotor activity, changes in purine levels, and adenosine receptors density in a ketamine-induced model of mania in rats. Inosine pretreatment (25 mg/kg, oral route) prevented the hyperlocomotion induced by ketamine (25 mg/kg, intraperitoneal route) in the open-field test; however, there was no difference in hippocampal density of A1 and A2A receptors, where ketamine, as well as inosine, were not able to promote changes in immunocontent of the adenosine receptors. Likewise, no effects of inosine pretreatments or ketamine treatment were observed for purine and metabolic residue levels evaluated. In this sense, we suggest further investigation of signaling pathways involving purinergic receptors, using pharmacological strategies to better elucidate the action mechanisms of inosine on bipolar disorder. Despite the limitations, inosine administration could be a promising candidate for bipolar disorder treatment, especially by attenuating maniac phase symptoms, once it was able to prevent the hyperlocomotion induced by ketamine in rats.

Copyright © 2020 Elsevier B.V. All rights reserved.

KEYWORDS

Adenosinergic system; Inosine; Mania

Title

Inosine prevents hyperlocomotion in a ketamine-induced model of mania in rats.

Author

Camerini L1, Ardais AP1, Xavier J1, Bastos CR1, Oliveira S1, Soares MSP2, de Mattos BDS2, avila AA2, do Couto CAT2, Spanevello RM2, Pochmann D3, Moritz CEJ4, Porciúncula LO5, Figueiro F6, Kaster MP6, Ghisleni G7.

Publish date

2020 Apr 15


Description :

Inosine, an endogenous purine nucleoside, has immunomodulatory, neuroprotective, and analgesic properties. In vitro: Inosine has been shown to stimulate axonal growth in cell culture and promote corticospinal tract axons to sprout collateral branches after stroke, spinal cord injury and TBI in rodent models.[1] Inosine dose-dependently stimulates cAMP production mediated through the A2AR. Inosine dose-dependently induces A2AR-mediated ERK1/2 phosphorylation.[2] In vivo: The reference for Inosine is 1 or 10 mg/kg, i.p. Preventive treatment with inosine inhibits the development and progression of EAE in C57Bl/6 mice. neuroinflammation and demyelinating processes are blocked by inosine treatment. Additionally, inosine consistently inhibits IL-17 levels in peripheral lymphoid tissue, as well as IL-4 levels and A2AR up-regulation in the spinal cord, likely, through an ERK1-independent pathway. [3] inosine acting through adenosine receptors (ARs) exerts a wide range of anti-inflammatory and immunomodulatory effects in vivo. [2]