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Diclofensine Hcl buy in Portsmouth
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Diclofensine Hcl

Diclofensine Hcl

Code: Diclofensine Hcl
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131 USD
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  • 3668 USD/g  - from 25 g
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Technical characteristics
  • BrandDiclofensine Hcl
  • Country of manufactureUnited States
  • Density322.229 g/cm³
  • Melting pointN/A °C
  • Type of substanceSolid
  • Storage temperature-20 °C
  • Boiling pointN/A °C
  • ConsistencyPowder
  • Diclofensine Hcl99.8% pure
Description

25I-NBOMe (2C-I-NBOMe, Cimbi-5, also shortened to "25I", and colloquially referred to as "N-bomb"[4]) is a psychedelic drug and derivative of the substituted phenethylamine psychedelic 2C-I. It was discovered in 2003 by chemist Ralf Heim at the Free University of Berlin, who published his findings in his PhD dissertation.[5] The compound was subsequently investigated by a team at Purdue University led by David Nichols.[6]

The carbon-11 labelled version of 25I-NBOMe, [11C]Cimbi-5, was synthesized and validated as a radiotracer for positron emission tomography (PET) in Copenhagen.[7][8] Being the first 5-HT2A receptor full agonist PET radioligand, [11C]-CIMBI-5 shows promise as a more functional marker of these receptors, particularly in their high affinity states

Like other 2C-X-NBOMe molecules, 25I-NBOMe is a derivative of the 2C family of phenethylamines described by Alexander Shulgin in his book PiHKAL.[9][10] Specifically, 25I-NBOMe is an N-benzyl derivative of the phenethylamine molecule 2C-I, formed by adding a 2-methoxybenzyl (BnOMe) onto the nitrogen (N) of the phenethylamine backbone. This substitution significantly increases the potency of the molecule

25I-NBOMe acts as a highly potent full agonist for the human 5-HT2A receptor,[2][11] with a Ki of 0.044 nM, making it some sixteen times the potency of 2C-I itself at this receptor. A radiolabelled form of 25I-NBOMe can be used for mapping the distribution of 5-HT2A receptors in the brain.[3]

25I-NBOMe induces a head-twitch response in mice which is blocked completely by a selective 5-HT2A antagonist, suggesting its psychedelic effects are mediated by 5-HT2A. This study suggested that 25I-NBOMe is approximately 14-fold more potent than 2C-I in-vivo.[12]

While in-vitro studies showed that N-benzyl derivatives of 2C-I were significantly increased in potency compared to 2C-I, the N-benzyl derivatives of the related compound DOI were inactive.[13]

Ki values of the following targets were greater than 500 nM: 5-HT1A, D3, H2, 5-HT1D, α1A adrenergic, δ opioid, serotonin uptake transporter, 5-HT5A, 5-HT1B, D2, 5-HT7, D1, 5-HT3, 5-HT1E, D5, muscarinic M1-M5, H3, and the dopamine uptake transporter

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