Apomorphine  (Synonyms: (-)-Apomorphine)

Apomorphine ((-)-Apomorphine) is a potent dopamine receptor agonist. Apomorphine also inhibit MAO-A and MAO-B. Apomorphine exerts neuroprotective effect and can relax rat corpus cavernosum. Apomorphine can inhibit ROS production, DNA fragmentation and inibit JNK and ERK1/2 phosphorylation. Apomorphine can enhance degradation of intracellular Aβ40 and Aβ42, reduces tau protein levels and inhibit MMP-9 expression. Apomorphine is a highly potent radical scavenger and iron chelator. Apomorphine can be used for the researches of dementia, parkinson's disease, alzheimer disease, breast carcinoma, and erectile dysfunction^{[1][2][3][4][5][6][7]}.

Apomorphine (0-250 μM; 30 min) inhibits striatal MAO-A and MAO-B activities from C57BL mice with IC₅₀ values of 93 μM and 241 μM, respectively^[2].
Apomorphine is a highly potent radical scavenger and iron chelator with an IC₅₀ of 0.2-0.5 μM^[2].
Apomorphine (7.5-15 μM; 24 h) protects SH-SY5Y cells against 6-OHDA (HY-B1081)-induced cell death, ROS production and DNA fragmentation^[3].
Apomorphine (15 μM; 8-24 h) attenuates 6-OHDA-induced JNK phosphorylation in SH-SY5Y cells^[3].
Apomorphine (7.5-30 μM; 24 h) does not induce intracellular glutathione synthesis in SH-SY5Y cells^[3].
Apomorphine (10 μM; 2 h pre-incubation) significantly enhances degradation of intracellular Aβ40 and Aβ42 in SH-SY5Y cells, reversing MG132 (HY-13259)-mediated inhibition of Aβ breakdown^[4].
Apomorphine (2-10 μM) significantly increases intracellular 20S proteasome and IDE activity in SH-SY5Y cells, and partially reverses MG132-induced proteasome inhibition^[4].
Apomorphine (5-20 μM; 24 h) significantly protects SH-SY5Y cells from H₂O₂-induced cell death and reduces H₂O₂-mediated p53 protein elevation^[4].
Apomorphine (10-100 μM; 24 h) exhibits minimal cytotoxicity in MCF-7 human breast carcinoma cells at concentrations ≤25 μM, with a 25% reduction in cell viability observed at 50 μM^[5].
Apomorphine (10-40 μM; 24 h) potently inhibits TNF-α- and PMA (HY-18739)-induced MMP-9 secretion in MCF-7 human breast carcinoma cells without altering MMP-2 levels^[5].
Apomorphine (40 μM; 24 h) inhibits TNF-α-induced invasion by MCF-7 human breast carcinoma cells by 80%^[5].
Apomorphine (20-40 μM; 18 h) suppresses TNF-α-induced MMP-9 mRNA expression in MCF-7 human breast carcinoma cells^[5].
Apomorphine (10-40 μM; 6 h) suppresses TNF-α-induced nuclear translocation of the AP-1 subunit c-Jun in MCF-7 human breast carcinoma cells without altering NF-κB subunit p65 nuclear translocation^[5].
Apomorphine (10-40 μM; 15-30 min) and (40 μM; 15, 30 min) inhibits TNF-α-induced phosphorylation of ERK1/2 in MCF-7 human breast carcinoma cells without altering phosphorylation of JNK, p38, or Akt^[5].
Apomorphine (10⁻⁹-10⁻⁴ M) produces concentration-dependent relaxation of rat corpus cavernosum^[6].
Apomorphine (100 μM; 4 min) does not alter tissue cGMP or cAMP levels in Phenylephrine (HY-B0769)-precontracted isolated rat corpus cavernosum strips^[6].
Apomorphine (0-600 μM) induces C6 cells (EC₅₀ = 200 μM) and rat neuron death^[7].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Apomorphine (1.0 mg/kg; injection; daily; 6 days) significantly reverses Scopolamine (HY-N0296)-induced dementia-related memory impairment, oxidative stress, reduced AChE activity, and altered hippocampal biogenic amine levels in male Albino Wistar rats^[1].
Apomorphine (5-10 mg/kg; s.c.; daily; 5 days) protects against MPTP MPTP (HY-W114750)-induced dopaminergic neurotoxicity in male C57BL mice, with 10 mg/kg almost completely preventing striatal dopamine loss and maintaining tyrosine hydroxylase content at 66.1% of control^[2].
Apomorphine (5-10 mg/kg; s.c.; once weekly; 1 month) significantly improves short-term memory function and reduces intraneuronal Aβ, p-tau, p53, and HO-1 levels in 3xTg-AD mice^[4].
Apomorphine (10-1000 nmol; s.c.; single dose) produces erectile responses in awake rats^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

267.32

C₁₇H₁₇NO₂

58-00-4

Solid

Blue to blue-green

OC1=CC=C2C(C3=C4C(CCN(C)[C@]4([H])C2)=CC=C3)=C1O

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Ikram H, et al. Memory enhancing and neuroprotective effects of apomorphine in a rat model of dementia. Metab Brain Dis. 2024;39(6):1051-1063.  [Content Brief]

  [2]. Grünblatt E, et al. Apomorphine protects against MPTP-induced neurotoxicity in mice. Mov Disord. 1999;14(4):612-618.  [Content Brief]

  [3]. Hara H, et al. Apomorphine attenuates 6-hydroxydopamine-induced apoptotic cell death in SH-SY5Y cells. Redox Rep. 2003;8(4):193-197.  [Content Brief]

  [4]. Himeno E, et al. Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation. Ann Neurol. 2011;69(2):248-256.  [Content Brief]

  [5]. Jung YS, et al. Apomorphine suppresses TNF-α-induced MMP-9 expression and cell invasion through inhibition of ERK/AP-1 signaling pathway in MCF-7 cells. Biochem Biophys Res Commun. 2017;487(4):903-909.  [Content Brief]

  [6]. Matsumoto K, et al. Effects in vitro and in vivo by apomorphine in the rat corpus cavernosum. Br J Pharmacol. 2005;146(2):259-267.  [Content Brief]

  [7]. dos Santos El-Bachá R, et al. Toxic effects of apomorphine on rat cultured neurons and glial C6 cells, and protection with antioxidants. Biochem Pharmacol. 2001;61(1):73-85.  [Content Brief]