2-Aminoindane─A Kind of Aminoindane with Its Stimulant Properties

9 Responses

  1. psychoactive drug says:

    Chemistry
    2-AI, or 2-Aminoindane, is a structural analogue of amphetamine. It features the R3 terminal carbon of the propane chain of amphetamine bound to the benzene ring. This creates an indane group, a bicyclic moeity containing a benzene ring fused to a pentane ring. 2-AI contains an amino group NH2 bound to R2 of the indane ring thus giving it the name 2-aminoindane. 2-AI is structurally analogous to NM-2-AI, lacking the N-substituted methyl group.

    Pharmacology
    Due to the lack of research regarding the substance, all discussion regarding the pharmacology of it is purely based upon its structure and subjective effect similarities to other stimulants such as amphetamine, methamphetamine and 2-FMA. 2-AI most likely acts as both a dopamine and norepinephrine releasing agent. This means it effectively boosts the levels of the norepinephrine and dopamine neurotransmitters in the brain by binding to and partially blocking the transporter proteins that normally remove those monoamines from the synaptic cleft. This allows dopamine and norepinephrine to accumulate within the brain, resulting in stimulating and euphoric effects.

  2. Description says:

    BACKGROUND OF THE INVENTION This invention novel naphthylethyl urea and naphthyl ethyl thiourea, process for their preparation, and to pharmaceutical compositions comprising them.
    Naphthylethyl urea with BACKGROUND ART Anti-hypercholesterolemic the literature, in particular the closest prior art E
    It is known from P344 425.
    The applicant has now discovered a novel compound that has a strong and significant property of specifically binding to melatonin receptors. These compounds due to the nature of their antagonize or action on melatonin has many pharmacological actions valuable. With physical action.
    In addition to their beneficial effects on disorders and sleep disorders and seasonal disorders of the circadian rhythm, they are the central nervous system, especially anxiolytic, anti-psychotic, and to a analgesic, as well as ovulation, cerebral circulation and with pharmacologically valuable properties relates immunomodulation.

  3. Application says:

    2-Aminoindan may be used to prepare trans-(1S,2S)-2-amino-1-indanol via hydroxylation using dopamine β-hydroxylase (DBH) enzyme.[3] It may be used to synthesize 2-amino-4-chloro-6-(2-aminoindanyl)-1,3,5-triazine

  4. General description says:

    2-Aminoindan (2-Aminoindane) is an analog of amphetamine. It shows a potential bronchodilator and analgesic effect.[1] The impact of the intramolecular N-H···Π hydrogen bonding on the conformations of 2-Al has been analyzed.

  5. Conformations of 2-aminoindan in a supersonic jet: the role of intramolecular N-H...pi hydrogen bonding. says:

    Laser-induced fluorescence (LIF), dispersed fluorescence (DF), mass-resolved one-color resonance enhanced two-photon ionization (RE2PI) and UV-UV hole-burning spectra of 2-aminoindan (2-AI) were measured in a supersonic jet. The hole-burning spectra demonstrated that the congested vibronic structures observed in the LIF excitation spectrum were responsible for three conformers of 2-AI. The origins of the conformers were observed at 36931, 36934, and 36955 cm(-1). The DF spectra obtained by exciting the band origins of the three conformers showed quite similar vibrational structures, with the exception of the bands around 600-900 cm(-1). The molecular structures of the three conformers were assigned with the aid of ab initio calculations at the MP2/6-311+G(d,p) level. An amino hydrogen of the most stable conformer points toward the benzene ring. The stability of the most stable conformer was attributed to an intramolecular N-H…pi hydrogen bonding between the hydrogen atom and the pi-electron of the benzene ring. The other two conformers, devoid of intramolecular hydrogen bonding, were also identified for 2-AI. This suggests weak hydrogen bonding in the most stable conformer. The intramolecular N-H…pi hydrogen bonding in 2-AI was discussed in comparison with other weak hydrogen-bonding systems.

  6. The neuroprotective mechanism of 1-(R)-aminoindan, the major metabolite of the anti-parkinsonian drug rasagiline. says:

    The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities. A prospective clinical trial has shown that rasagiline confers significant symptomatic improvement and demonstrated alterations in Parkinson’s disease progression. Rasagiline is primarily metabolized by hepatic cytochrome P-450 to form its major metabolite, 1-(R)-aminoindan, a non-amphetamine, weak reversible MAO-B inhibitor compound. Recent studies indicated the potential neuroprotective effect of 1-(R)-aminoindan, suggesting that it may contribute to the overall neuroprotective and antiapoptotic effects of its parent compound, rasagiline. This review article briefly highlights the molecular mechanisms underlying the neuroprotective properties of the active metabolite of rasagiline, 1-(R)-aminoindan, supporting the valuable potential of rasagiline for disease modification.

  7. Availability and Supply of Novel Psychoactive Substances says:

    Numerous factors hinder the adequate characterisation of the availability and supply of novel psychoactive substances (NPS). Diverse substances – botanicals; synthetic cannabinoid receptor agonists (SCRAs); cathinone analogues; pyrrolidinophenones; substituted phenylethylamines; ‘FLYs;’ piperazines; aminoindanes; and analogues of tryptamines, arylcyclohexylamines, opioids, cocaine, and gamma-hydroxybutyrate – compete in a shifting market space, defying generalisations. ‘Supply side’ analysis is complicated by ongoing market entries, including compounds, suppliers, distributors and vendors. Recent years have witnessed an exceptional surge of entirely new psychoactive substances. Online platforms for NPS transactions have flourished, complimented by increasing product diversity [1,2].

    Evolving usage patterns in various nationalities or communities (‘demand side’), coupled with assorted market stressors, ensure a constantly shifting landscape. NPS compete with other established abused substances for selection, as well as for available interventions and treatment resources. User experiences, perceptions of harm and purchasing sources are rapidly disseminated via various social media. The legal, administrative and regulatory environments continue to evolve at local, state, national and transnational levels, often in a reactionary manner. Medical or forensic analysis, characterisation, detection and measurement in patient biological specimens or product samples are complicated by deficiencies in widely available, validated methodologies or established reference standards.

    Further adding to the difficulties of NPS market assessment is the fact that much NPS development, production and introduction is unlinked from traditional avenues and pressures. Marijuana, cocaine, heroin, khat, peyote and psilocybin mushrooms (as well as nicotine and grain or fruit sources for ethanol production) require some degree of cultivation or rendering. Unlike ketamine, or prescribed opioids, benzodiazepines, or amphetamines analogues, numerous NPS do not possess the legal exposure derived from diversion from legitimate sources. Similar to amphetamine-type stimulants (ATS) and synthetic opioids, many NPS are completely divorced from botanical origins, requiring only knowledge, materials, standard laboratory equipment and a relatively brief production cycle. Additionally, NPS remain largely free from the national and international efforts targeting precursor chemicals and ATS and non-pharmaceutical opioid reagents (e.g., The Combat Methamphetamine Epidemic Act of 2005, 1988 United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychoactive Substances, Drug Enforcement Administration (DEA) fentanyl chemical precursor scheduling, etc.) [3–5].

    Classical data sources struggle to address the NPS hyperkinetic market. Inherent delays in the conduct of research, (peer) review and production limit journal publications, books and reports. The surreptitious ‘shadow economy’ surrounding NPS and the absence of accessible, complete, recorded sources preclude a conventional ‘market research report’ analysis. Traditional databases assessing usage and demand often do not include NPS or update recent introductions with adequate frequency. For example, through July 2012, usage statistics for kratom (Mitragyna speciosa), SCRAs, cathinones, piperazines, or ring-substituted phenylethylamines were unavailable in recent US Drug Abuse Warning Network (DAWN), National Survey on Drug Use and Health, or the Youth Risk Behavior Surveillance Systems databases [6–8]. Drugs of abuse classifications often maintain broad, historical categories inapplicable to NPS. The 2012 DAWN report of drug-related emergency department visits, summarising 2010 data, continued to employ such traditional categorisations [7]. SCRA data were unaddressed until the 2011 Monitoring The Future study (published 2012); cathinones and other NPS were absent [9]. DEA drug seizures, mostly recently available for 2010, reflect only cocaine, heroin, marijuana, methamphetamine and ‘hallucinogens’ [10]. Available European (EMCDDA) seizure data, mostly recently from 2009, are similarly constrained by category limitations [11]. While the US National Poison Data System (NPDS) identified emerging trends for SCRAs and cathinones in 2009, formal publication (non-blogs or press releases) occurred in 2011 [12]. Other flexible data systems and organisations have fallen victim to economic constraints. The US National Drug Intelligence Center ceased operation of its Synthetic Drug Early Warning and Response System (SENTRY) on November 1, 2011 and itself folded on June 15, 2012.

  8. Detection of mismatched nucleotides in dsDNA. says:

    This technique is based on the fact that a DNA ligase can covalently join two oligonucleotides when they are hybridized immediately adjacent to each other on a complementary DNA. When the nucleotide(s) at the junction is incorrectly base paired, for example, due to a point mutation (as in human β-globin alleles responsible for sickle cell anemia), the efficiency of ligase-mediated phosphodiester bond formation decreases substantially. This distinction, especially when combined with the ligase-based gene amplification techniques described earlier, provides a sensitive mutant gene detection method which can be applied to the diagnosis of a variety of viral and genetic diseases (33–35).

    A significant improvement to this ligation amplification and mismatch detection system is the introduction of thermostable DNA ligase, for example, from T. aquaticus (36). The use of thermostable DNA ligase simplifies the repetitive thermal cycles, as does the thermostable DNA polymerase in PCR, and also significantly improves the mismatch discrimination due to the high ligation temperature (65°C).

  9. Synthesis of long RNA molecules. says:

    The capacity of the T4 DNA ligase to ligate RNA junctions in double-stranded regions enables one to prepare long RNA molecules in a highly efficient and selective manner (43). Compared with the RNA ligation that can be performed using the T4 RNA ligase (see Section II, this chapter), the T4 DNA ligase offers the following advantages.

    (a) The low Km of the T4 DNA ligase for double-stranded polynucleotides (from 10”8 to IGT7 M) permits efficient ligations to be performed at submicromolar to micromolar concentrations of RNA instead of the millimolar range of concentrations required for T4 RNA ligase.

    (b) The T4 DNA ligase produces RNA ligation at a substantially higher specificity due to the requirement for double-stranded template structure. Thus side products such as circular and oligomeric RNA molecules are not generated even when the 3′-OH terminus of the phosphate donor RNA is not protected. In case RNA substrates are synthesized by in vitro transcription with T7, T3, or SP6 RNA polymerases (see Section I, Chapter 7), the by-products carrying an extra nontemplated nucleotide at the 3′ terminus (N + 1 products) are efficiently discriminated against the correct acceptor molecules (N products), reducing the possibility of mismatching nucleotide insertions.

Leave a Reply

Your email address will not be published. Required fields are marked *