6-ohda

Oxidopamine hydrobromide (6-OHDA hydrobromide) is a widely used neurotoxin and an antagonist of the neurotransmitter dopamine. It selectively destroys dopaminergic neurons, promotes COX-2 activation, induces PGE2 synthesis, and stimulates the secretion of the pro-inflammatory cytokine IL-1β. It is commonly used to establish animal models of Parkinson’s disease (PD).

Oxidopamine hydrochloride (6-Hydroxydopamine hydrochloride) is a widely used neurotoxin and an antagonist of the neurotransmitter dopamine. It selectively destroys dopaminergic neurons, promotes COX-2 activation, induces PGE2 synthesis, and stimulates the secretion of the inflammatory cytokine IL-1β. It is commonly used to establish animal models of Parkinson’s disease (PD).

Propargyl-PEG3-acid is a non-cleavable (3-unit PEG) ADC linker and a PEG-based PROTAC linker, used to synthesize 6-OHDA-PEG3-yne, a compound containing 6-OHDA and Propargyl-PEG3-acid[1].

Sesaminol is an orally active activator of the Nrf2-ARE signaling pathway, promoting the nuclear translocation of Nrf2 and boosting the expression of NQO1 to enhance cellular defense against oxidative stress. It inhibits 6-OHDA-induced ROS production and apoptosis in SH-SY5Y cells. Sesaminol also provides neuroprotective effects against Rotenone-induced Parkinson's disease.

A-86929 is a potent and selective dopamine D1 receptor agonist with a pKi of 7.3. It significantly induces rotational behavior in a 6-OHDA-induced unilateral nigral lesion rat model and improves motor function in an MPTP-induced Parkinson's disease marmoset model. Furthermore, A-86929 shows potential value in reducing cocaine-induced craving behavior in rats and reversing Haloperidol-induced cognitive deficits in rhesus monkeys. The compound is useful for researching neurological disorders.

BChE/MAO-B-IN-1 is a dual inhibitor of BChE and MAO-B, with IC50 values of 375 nM and 20 nM, respectively. It effectively counteracts oxidative damage induced by H2O2 and 6-OHDA in SH-SY5Y cells and can penetrate the central nervous system in cell models simulating the blood-brain barrier. BChE/MAO-B-IN-1 is applicable for research into neurological disorders such as Alzheimer's disease (AD).

Dual AChE-MAO B-IN-4 (compound 7) is a dual inhibitor of AChE and MAO-B, with IC50 values of 261 nM and 15 nM, respectively. It offers protection against oxidative damage induced by H2O2 and 6-OHDA in SH-SY5Y cells and can penetrate the central nervous system in a model simulating the blood-brain barrier. This compound is applicable in research on neurological disorders such as Alzheimer's disease (AD).

SKF-80723 HBr is a D1 receptor agonist. SKF-80723 HBr strongly potentiated the contralateral circling induced by quinpirole in rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of the medial forebrain bundle.

C-DIM12 induced expression of Nurr1-regulated genes. C-DIM12 increased expression of transfected human Nurr1, induced Nurr1 protein expression in primary dopaminergic neurons and enhanced neuronal survival from exposure to 6-OHDA.

Danshensu has antioxidant activity, can enhance HO-1 expression to suppress 6-OHDA-induced oxidative damage via PI3K/Akt/Nrf2 signaling pathways.

Amifostine thiol (WR-1065) is a radioprotectant that protects DNA from fast neutron-induced strand breaks.Amifostine thiol ameliorates (P<0.001) 6-OHDA-induced stiffness in a dose-dependent manner and activates p53 through a JNK-dependent signaling pathway.

Pinostilbene obviously attenuates the phosphorylation of c-Jun and JNK triggered by 6-OHDA.

D-DOPA is an enantiomer of the dopamine precursor L-DOPA . It can be converted to L-DOPAviasequential oxidation and transamination, which are mediated by D-amino acid oxidase (DAAO) and DOPA transaminase, respectively, in rat kidney homogenates.1It reduces the number of dopaminergic neurons in primary rat embryonic mesencephalic cultures in a concentration-dependent manner.2Intraventricular administration of D-DOPA (200 μg/animal) increases striatal dopamine levels in rats.3D-DOPA (20 mg/kg, i.p.) induces contralateral turns in a rat model of Parkinson's disease induced by 6-OHDA .4 1.Wu, M., Zhou, X.-J., Konno, R., et al.D-dopa is unidirectionally converted to L-dopa by D-amino acid oxidase, followed by dopa transaminaseClin. Exp. Pharmacol. Physiol.33(11)1042-1046(2006) 2.Ling, Z.-D., Pieri, S.C., and Carvey, P.M.Comparison of the neurotoxicity of dihydroxyphenylalanine stereoisomers in cultured dopamine neuronsClin. Neuropharmacol.19(4)360-365(1996) 3.Karoum, F., Freed, W.J., Chuang, L.-W., et al.D-dopa and L-dopa similarly elevate brain dopamine and produce turning behavior in ratsBrain Res.440(1)190-194(1988) 4.Moses, J., Siddiqui, A., and Silverman, P.B.Sodium benzoate differentially blocks circling induced by D-and L-dopa in the hemi-parkinsonian ratNeurosci. Lett.218(3)145-148(1996)

1. beta-Asarone (Cis-Isoelemicin) may be a potential preventive drug for Alzheimer's disease. 2. Beta-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in SAMP8 mice. 3. The co-administration of beta-Asarone(Cis-Isoasarone) and l-dopa may contribute to the treatment of 6-OHDA-induced damage in rats by inhibiting autophagy activity. 4. Beta-Asarone exhibits anti-inflammatory effects by suppressing the production of pro-inflammatory mediators through NF-κB signaling and the JNK pathways in activated microglial cells and might be developed as a promising candidate to treat various neuroinflammatory diseases.

1. 5,7-Dihydroxychromone (5,7-Dihydroxy-4H-Chromen-4-One) isolated from DME is one of the active compounds that may contribute to regulate blood glucose levels. 2. 5,7-Dihydroxychromone exerts neuroprotective effect against 6-OHDA-induced oxidative stress and apoptosis by activating Nrf2/ARE signal . 3. 5,7-Dihydroxychromone induces the translocation of Nrf2 to the nucleus and increases Nrf2/ARE binding activity which results in the up-regulation of the expression of Nrf2-dependent antioxidant genes, including HO-1, NQO1, and GCLc.

Notoginsenoside R2 (20(S)-Notoginsenoside R2) has neuroprotection against 6-OHDA-induced neurotoxicity, is associated with Notoginsenoside R2-mediated P90RSK and Nrf2 activation through MEK1/2-ERK1/2 pathways.

GSK3-IN-3 is a mitochondrial autophagy (mitophagy) inducer and GSK-3 inhibitor (IC50: 3.01 μM) that induces parkin-dependent mitochondrial autophagy. GSK3-IN-3 is non-ATP and non-substrate competitive and neuroprotective against 6-OHDA.

Isoasiaticoside, a pentacyclic triterpene saponin derived from Centella asiatica, exhibits potential neuroprotective effects in the 6-OHDA-induced PC12 cell model [1].

Inubritannolide A exhibits moderate to robust neuroprotective effects across various neuronal cell types against inducers such as H2O2, 6-hydroxydopamine (6-OHDA), and lipopolysaccharide (LPS).

NOP agonist-1 (compound 4) is a nociceptin opioid receptor (NOP) partial agonist that attenuates Parkinsonian disabilities in 6-OHDA hemilesioned rats [1].

PQM-164 (Compound 3e) exhibits antioxidative properties, demonstrated by its ability to scavenge DPPH free radicals with an IC50 of 0.93 μM. This compound shows anti-inflammatory activity against neuronal damage induced by activated microglia due to 6-OHDA. Additionally, PQM-164 reduces the accumulation of α-synuclein and enhances the nuclear translocation and transcriptional activity of Nrf2. PQM-164 is utilized in research related to Parkinsons disease.

5,7-Dihydroxychromone (Standard) is a reference standard for research and analysis in studies involving 5,7-Dihydroxychromone. 1. 5,7-Dihydroxychromone (5,7-Dihydroxy-4H-Chromen-4-One) isolated from DME is one of the active compounds that may contribute to regulate blood glucose levels. 2. 5,7-Dihydroxychromone exerts neuroprotective effect against 6-OHDA-induced oxidative stress and apoptosis by activating Nrf2/ARE signal . 3. 5,7-Dihydroxychromone induces the translocation of Nrf2 to the nucleus and increases Nrf2/ARE binding activity which results in the up-regulation of the expression of Nrf2-dependent antioxidant genes, including HO-1, NQO1, and GCLc.

beta-Asarone (Standard) is a reference standard for research and analysis in studies involving beta-Asarone. 1. beta-Asarone (Cis-Isoelemicin) may be a potential preventive drug for Alzheimer's disease. 2. Beta-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in SAMP8 mice. 3. The co-administration of beta-Asarone(Cis-Isoasarone) and l-dopa may contribute to the treatment of 6-OHDA-induced damage in rats by inhibiting autophagy activity. 4. Beta-Asarone exhibits anti-inflammatory effects by suppressing the production of pro-inflammatory mediators through NF-κB signaling and the JNK pathways in activated microglial cells and might be developed as a promising candidate to treat various neuroinflammatory diseases.

Notoginsenoside R2 (Standard) is a reference standard for research and analysis in studies involving Notoginsenoside R2. Notoginsenoside R2 (20(S)-Notoginsenoside R2) has neuroprotection against 6-OHDA-induced neurotoxicity, is associated with Notoginsenoside R2-mediated P90RSK and Nrf2 activation through MEK1/2-ERK1/2 pathways.