| Stereochemistry | RACEMIC |
| Molecular Formula | C9H9NO3 |
| Molecular Weight | 179.1727 |
| Optical Activity | ( + / - ) |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CN1CC(O)C2=CC(=O)C(=O)C=C12
InChI
InChIKey=RPHLQSHHTJORHI-UHFFFAOYSA-N
InChI=1S/C9H9NO3/c1-10-4-9(13)5-2-7(11)8(12)3-6(5)10/h2-3,9,13H,4H2,1H3
Adrenochrome is a member of a class of chemicals known as aminochromes, each one derived by the oxidation of its precursor amine. Adrenochrome was proposed for the biogenesis of schizophrenia in 1952. Since that time the adrenochrome theory has been one of the most established and discussed theories in this field. It is known, that adrenochrome is toxic to myocar-dial tissue and may be responsible for fibril-lation and sudden death under stress. Aminochrome has been suggested as a physiological preclinical model capable of inducing five of the six mechanisms of Parkinson's disease. Until now, there is no evidence that aminochrome induces glial activation related to neuroinflammation, an important mechanism involved in the loss of dopaminergic neurons, but was shown, aminochrome neuroinflammatory ability and supported the hypothesis that it might be a better PD preclinical model to find new pharmacological treatment that stop the development of this disease.
CNS Activity
Originator
Approval Year
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
PubMed
Patents
Sample Use Guides
Aminochrome was found to be toxic in a mouse-derived neuronal cell line (CNh). The effect was concentration dependent (10-150 microM). The issue whether aminochrome toxicity involves glutamate transmission was studied with several glutamate receptors antagonists. Incubation of the cells with aminochrome (150 microM) in the presence of 100 microM of the AMPA antagonist, NBQX resulted in an increase of cell survival, from 52 to 73%. However, this protective effect did not seem to be related to activation of ionotropic glutamate receptors since incubation of CNh cells with 200 microM of glutamate resulted in only 10% decrease of cell survival. However, NBQX was found to inhibit in vitro the autoxidation process. One hundred microM AP-5 did not have any effect on aminochrome toxicity. The toxic effect of aminochrome on CNh cells seems to be dependent of extracellular activation since addition of dicoumarol, a specific inhibitor of DT-diaphorase, did not affect that toxicity, which can be explained perhaps by a lack of a transport system for aminochrome into the CNh cells.
SUBSTANCE RECORD
