(-)-Butaclamol hydrochloride - CAS 55528-08-0
Category:
Main Product
Product Name:
(-)-Butaclamol hydrochloride
Catalog Number:
55528-08-0
Synonyms:
(-)-Butaclamolhydrochloride; BUTACLAMOLHYDROCHLORIDE; 55528-08-0; ButaclamolHCl; Butaclamolhydrochloride(USAN); Butaclamolhydrochloride[USAN]
CAS Number:
55528-08-0
Molecular Weight:
397.98
Molecular Formula:
C25H32ClNO
COA:
Inquire
MSDS:
Inquire
Canonical SMILES:
CC(C)(C)C1(CCN2CC3C4=CC=CC=C4CCC5=C3C(=CC=C5)C2C1)O.Cl
InChI:
InChI=1S/C25H31NO.ClH/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;1H/t21-,22-,25-;/m1./s1
InChIKey:
QZRUMKUMFJJARD-OMMJFLKZSA-N
Chemical Structure
CAS 55528-08-0 (-)-Butaclamol hydrochloride

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.Acute administration of dopaminergic drugs has differential effects on locomotion in larval zebrafish.
Irons TD1, Kelly PE, Hunter DL, Macphail RC, Padilla S. Pharmacol Biochem Behav. 2013 Feb;103(4):792-813. doi: 10.1016/j.pbb.2012.12.010. Epub 2012 Dec 28.
Altered dopaminergic signaling causes behavioral changes in mammals. In general, dopaminergic receptor agonists increase locomotor activity, while antagonists decrease locomotor activity. In order to determine if zebrafish (a model organism becoming popular in pharmacology and toxicology) respond similarly, the acute effects of drugs known to target dopaminergic receptors in mammals were assessed in zebrafish larvae. Larvae were maintained in 96-well microtiter plates (1 larva/well). Non-lethal concentrations (0.2-50 μM) of dopaminergic agonists (apomorphine, SKF-38393, and quinpirole) and antagonists (butaclamol, SCH-23390, and haloperidol) were administered at 6 days post-fertilization (dpf). An initial experiment identified the time of peak effect of each drug (20-260 min post-dosing, depending on the drug). Locomotor activity was then assessed for 70 min in alternating light and dark at the time of peak effect for each drug to delineate dose-dependent effects.
3.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.
4.[Role of DopR in the molecular mechanism of the dopamine control of juvenile hormone metabolism in female Drosophila].
Karpova EK, Bogomolova EV, Romonova IV, Gruntenko NE, Raushenbakh IIu. Genetika. 2012 Aug;48(8):999-1002.
The effect of a decreased availability of the D1-like dopamine receptor (DopR) in Drosophila (caused by DopR antagonist added into food) on the juvenile hormone (JH) synthesis rate in young female D. melanogaster has been studied. The JH degradation rate and the alkaline phosphatase (ALP) and tyrosine decarboxylase (TDC) activities were used as indicators of the JH synthesis rate. Treatment of the flies with butaclamol, a specific DopR antagonist, has been demonstrated to increase the JH degradation rate, and the stress reactivity of the system of JH metabolism and decrease the ALP activity and stress reactivity, and increase the TDC activity and stress reactivity. As shown earlier, all this indicates a decrease in the JH synthesis rate in young female drosophila with a decreased DopR availability. It is concluded that the activating effect of dopamine on JH synthesis in Drosophila is mediated by D1-like receptors.