MCE products for research use only. We do not sell to patients.

Oxidopamine hydrochloride

MCE China：Oxidopamine hydrochloride

Brand：MedChemExpress (MCE)

Cat. No.HY-B1081

CAS：28094-15-7

Synonyms：6-Hydroxydopamine Hydrochloride

Purity：99.71%

Storage：4°C, stored under nitrogen *The compound is unstable in solutions, freshly prepared is recommended.

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Oxidopamine (6-OHDA) hydrochloride is an antagonist of the neurotransmitter dopamine. Oxidopamine hydrochloride is a widely used neurotoxin and selectively destroys dopaminergic neurons. Oxidopamine hydrochloride promotes COX-2 activation, leading to PGE2 synthesis and pro-inflammatory cytokine IL-1β secretion. Oxidopamine hydrochloride can be used for the research of Parkinson’s disease (PD), attention-deficit hyperactivity disorder (ADHD), and Lesch-Nyhan syndrome.

In Vitro：Oxidopamine hydrochloride (0-500 μM, 24 h) decreases the viability of both Neuro-2a cells and SH-SY5Y cells in a concentration-dependent manner[1]. Oxidopamine hydrochloride (75-150 μM, 0-24 h) induces COX-2 expression and nuclear translocation[1]. Oxidopamine hydrochloride (75-150 μM, 0-24 h) causes PGE2 biosynthesis and pro-inflammatory cytokine IL-1β production[1]. Oxidopamine hydrochloride (0-150 μM, 12 h) induces apoptosis and mitochondrial membrane depolarization of pheochromocytoma PC12 cells[3]. Oxidopamine hydrochloride (75 μM, 0-12 h) induces p38 phosphorylation[3].

In Vivo：Oxidopamine (6-OHDA) hydrochloride can induce Parkinson's disease models[5][6]. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction ofParkinson's disease model[5][6] Background The chemical structure of Oxidopamine (6-OHDA) hydrochloride is similar to dopamine (DA), enabling it to compete with DA for uptake sites and be subsequently taken into cells. Once inside the cells, oxidopamine hydrochloride can be oxidized and decomposed, generatingreactive oxygen species, which further produce oxygen free radicals through MAO (monoamine oxidase) or directly cause mitochondrial dysfunction, leading to thedeath of dopaminergic neurons. Specific Mmodeling Methods Rat: Sprague-Dawley (SD) • Male • 200-250g • Administration: 5μg/2μL/site • stereotaxicallyinjected in the fight striatum • single dose. Note (1) Lesions were made by the unilateral injection of Oxidopamine hydrochloride (5 μg in 2 μl/site) into the right striatum at the two coordinates: ① AP, ?0.7; L, ?3.0; DV, ?5.5 and 4.5 mm from Bregma. ② AP, ?0.2; L, ?2.6; DV, ?5.5 and 4.5 mm from Bregma.The two coordinates were injected Oxidopamine hydrochloride 10 μg in 4 μl/2 sites.(2) Oxidopamine hydrochloride was prepared freshly in dark to avoid autooxidation, and was administered using a 5 μl microinjector at a rate of 0.5 μl/min. The syringe was left in place for 5 min before slowly retracting it to allow for toxin diffusion and prevent the toxin reflux.(3) On the 56th day after the injury, the animals were decapitated under deep halothane anesthesia. Their brains were quickly removed from the skull, rinsed with chilled saline, and tissue samples containing the caudate-putamen head were dissected from both the lesioned and unlesioned striata on ice.(4) The animals were housed in an environment with a 12-hour light/dark cycle, with the temperature maintained at 22-23°C. They were allowed free access to food and tap water. Modeling Indicators Behavioral monitoring: Rats exhibit rotation with a rotation count greater than 210 r/30 min.Molecular changes: Elevated levels of COX-2, TNF-α mRNA, and COX-2 protein.Histopathological changes: Chromatin condensation into clumps around the nucleus, along with evident mitochondrial swelling and vacuolation. Induced nigrostriatal nerve terminal lesions. Decreased striatal dopamine levels and reduced number of tyrosine hydroxylase immunoreactive cells in the ipsilateral substantia nigra, accompanied by long-term significant atrophy of remaining dopaminergic neurons. Correlated Product(s): / Opposite Product(s): Resveratrol (HY-16561)

IC50 & Target：COX-2 IL-1β Caspase-3 Caspase-8 Caspase-9

Hot selling product：Anifrolumab  | Sitagliptin  | AVE 0991  | SB 525334  | GSK682753A  | OSS_128167  | L-Arginine  | L-Glutamine  | SKL2001  | DL-Isocitric acid (trisodium salt)

Trending products：Recombinant Proteins  |  Bioactive Screening Libraries  |  Natural Products  |  Fluorescent Dye  |  PROTAC  |  Isotope-Labeled Compounds  |  Oligonucleotides

References：

[1]. Kang X, et al. Cyclooxygenase-2 contributes to oxidopamine-mediated neuronal inflammation and injury via the prostaglandin E2 receptor EP2 subtype. Sci Rep. 2017 Aug 25;7(1):9459.  [Content Brief]

[2]. Jin F, et al. Neuroprotective effect of resveratrol on 6-OHDA-induced Parkinson's disease in rats. Eur J Pharmacol. 2008 Dec 14;600(1-3):78-82.  [Content Brief]

[3]. Fujita H et al. Cell-permeable cAMP analog suppresses 6-hydroxydopamine-induced apoptosis in PC12 cells through the activation of the Akt pathway. Brain Res. 2006 Oct 3;1113(1):10-23.  [Content Brief]

[4]. Soto-Otero R et al. Autoxidation and neurotoxicity of 6-hydroxydopamine in the presence of some antioxidants: potential implication in relation to the pathogenesis of Parkinson's disease. J Neurochem. 2000 Apr;74(4):1605-12.  [Content Brief]