(+)-Butaclamol - CAS 56245-67-1
Category:
Main Product
Product Name:
(+)-Butaclamol
Catalog Number:
56245-67-1
Synonyms:
(+)-Butaclamol;d-Butaclamol;BUTACLAMOL;CHEMBL8514;Butaclamolum;1H-Benzo(6,7)cyclohepta(1,2,3-de)pyrido(2,1-a)isoquinolin-3-ol,2,3,4,4a,8,9,13b,14-octahydro-3-(1,1-dimethylethyl)-,(3S-(3-alpha,4a-alpha,13b-beta))-
CAS Number:
56245-67-1
Molecular Weight:
361.51974;g/mol
Molecular Formula:
C25H31NO
COA:
Inquire
MSDS:
Inquire
Canonical SMILES:
CC(C)(C)C1(CCN2CC3C4=CC=CC=C4CCC5=C3C(=CC=C5)C2C1)O
InChI:
InChI=1S/C25H31NO/c1-24(2,3)25(27)13-14-26-16-21-19-9-5-4-7-17(19)11-12-18-8-6-10-20(23(18)21)22(26)15-25/h4-10,21-22,27H,11-16H2,1-3H3/t21-,22-,25-/m0/s1
InChIKey:
ZZJYIKPMDIWRSN-HWBMXIPRSA-N
Chemical Structure
CAS 56245-67-1 (+)-Butaclamol

Reference Reading


1.Arylpiperazine dopamineric ligands protect neuroblastoma cells from nitric oxide (NO)-induced mitochondrial damage and apoptosis.
Tovilovic G1, Zogovic N, Harhaji-Trajkovic L, Misirkic-Marjanovic M, Janjetovic K, Vucicevic L, Kostic-Rajacic S, Schrattenholz A, Isakovic A, Soskic V, Trajkovic V. ChemMedChem. 2012 Mar 5;7(3):495-508. doi: 10.1002/cmdc.201100537. Epub 2012 Feb 1.
The protective ability of novel arylpiperazine-based dopaminergic ligands against nitric oxide (NO)-mediated neurotoxicity is investigated. The most potent neuroprotective arylpiperazine identified during the study was N-{4-[2-(4-phenyl-piperazin-1-yl)ethyl]-phenyl}picolinamide, which protected SH-SY5Y human neuron-like cells from the proapoptotic effect of NO donor sodium nitroprusside (SNP) by decreasing oxidative stress, mitochondrial membrane depolarization, caspase activation and subsequent phosphatydilserine externalization/DNA fragmentation. The protective effect was associated with the inhibition of proapoptotic (JNK, ERK, AMPK) and activation of antiapoptotic (Akt) signaling pathways, in the absence of interference with intracellular NO accumulation. The neuroprotective action of arylpiperazines was shown to be independent of dopamine receptor binding, as it was not affected by the high-affinity D₁/D₂ receptor blocker butaclamol.
2.Dopamine and T cells: dopamine receptors and potent effects on T cells, dopamine production in T cells, and abnormalities in the dopaminergic system in T cells in autoimmune, neurological and psychiatric diseases.
Levite M1,2,3. Acta Physiol (Oxf). 2016 Jan;216(1):42-89. doi: 10.1111/apha.12476. Epub 2015 Sep 24.
Dopamine, a principal neurotransmitter, deserves upgrading to 'NeuroImmunotransmitter' thanks to its multiple, direct and powerful effects on most/all immune cells. Dopamine by itself is a potent activator of resting effector T cells (Teffs), via two independent ways: direct Teffs activation, and indirect Teffs activation by suppression of regulatory T cells (Tregs). The review covers the following findings: (i) T cells express functional dopamine receptors (DRs) D1R-D5R, but their level and function are dynamic and context-sensitive, (ii) DR membranal protein levels do not necessarily correlate with DR mRNA levels, (iii) different T cell types/subtypes have different DR levels and composition and different responses to dopamine, (iv) autoimmune and pro-inflammatory T cells and T cell leukaemia/lymphoma also express functional DRs, (v) dopamine (~10(-8) M) activates resting/naive Teffs (CD8(+) >>>CD4(+) ), (vi) dopamine affects Th1/Th2/Th17 differentiation, (vii) dopamine inhibits already activated Teffs (i.
3.Stimulants as specific inducers of dopamine-independent σ agonist self-administration in rats.
Hiranita T1, Soto PL, Tanda G, Kopajtic TA, Katz JL. J Pharmacol Exp Ther. 2013 Oct;347(1):20-9. doi: 10.1124/jpet.113.207522. Epub 2013 Aug 1.
A previous study showed that cocaine self-administration induced dopamine-independent reinforcing effects of σ agonists mediated by their selective actions at σ1 receptors (σ1Rs), which are intracellularly mobile chaperone proteins implicated in abuse-related effects of stimulants. The present study assessed whether the induction was specific to self-administration of cocaine. Rats were trained to self-administer the dopamine releaser, d-methamphetamine (0.01-0.32 mg/kg per injection), the μ-opioid receptor agonist, heroin (0.001-0.032 mg/kg per injection), and the noncompetitive N-methyl-d-aspartate receptor/channel antagonist ketamine (0.032-1.0 mg/kg per injection). As with cocaine, self-administration of d-methamphetamine induced reinforcing effects of the selective σ1R agonists PRE-084 [2-(4-morpholinethyl)1-phenylcyclohexanecarboxylate hydrochloride] and (+)-pentazocine (0.032-1.0 mg/kg per injection, each). In contrast, neither self-administration of heroin nor ketamine induced PRE-084 or (+)-pentazocine (0.
4.Hetero-dimerization of serotonin 5-HT(2A) and dopamine D(2) receptors.
Lukasiewicz S1, Polit A, Kędracka-Krok S, Wędzony K, Maćkowiak M, Dziedzicka-Wasylewska M. Biochim Biophys Acta. 2010 Dec;1803(12):1347-58. doi: 10.1016/j.bbamcr.2010.08.010. Epub 2010 Sep 8.
In the present study, detailed information is presented on the hetero-dimerization of the serotonin 5-HT(2A) receptor and the dopamine D(2) receptor. Biophysical approaches (fluorescence spectroscopy as well as fluorescence lifetime microscopy) were used to determine the degree of fluorescence resonance energy transfer (FRET) between cyan and yellow fluorescent protein labeled receptor variants co-expressed in human embryonic kidney 293 cells (HEK293). Recorded data demonstrate the existence of energy transfer between the wild-type forms of 5-HT(2A)R and D(2)R, pointing toward the formation of hetero-5-HT(2A)R/D(2)R dimers and homo-5-HT(2A)R/5-HT(2A)R dimers. Moreover, the present study investigates the role of specific motifs (one containing adjacent arginine residues (217RRRRKR222) in the third intracellular loop (ic3) of D(2)R, and the other consisting of acidic glutamate residues (454EE455) in the C-tail of (5-HT(2A)R) in the formation of noncovalent complexes between these receptors.