Therapeutic agent composition and method of use

a technology of therapeutic agents and compositions, applied in the field of nmda ampa receptors, can solve the problems of degeneration and death of neurons, difficult to determine the optimal dosage or human treatment, and the bell-shaped curve model of rats may be only applied to rats, and may not be entirely appropriate for human applications. to achieve the effect of promoting myelin production

Inactive Publication Date: 2007-10-18
TRAN LOI H
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Excessive excitation by neurotransmitters can cause the degeneration and death of neurons.
Without the clear understanding of the mechanism of action of GPE, it was very difficult to determine the optimal dosage or human treatment.
The empirical bell-shaped curve-model for rats may be only applied to rats and might not be entirely appropriate for human applications.
Private communication with the Gluckman group showed unpublished results of recent studies in which high concentrations of GPE administered intraperitoneally and intravenously caused severe brain damage to rats.
It was questionable whether GPE may be a suitable neuroprotective agent based on unreproducible results of the bell-shaped curve concentrations of GPE.
It was found that increasing the dose to 100 μg or more usually killed the sheep fetus.

Method used

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  • Therapeutic agent composition and method of use
  • Therapeutic agent composition and method of use
  • Therapeutic agent composition and method of use

Examples

Experimental program
Comparison scheme
Effect test

experiment 1

[0094] Cyclic PG prevents glutamate induced neuronal death in vitro in a dose related manner.

Materials and Methods:

Cerebellar Cell Culture Preparing and coating of cover slips

[0095] Ten coverslips were placed into a large petri dish and washed in 70% alcohol for 5 minutes, then washed with Millipore H2O. The coverslips were air dried, then coated with Poly-D-Lysine (1 mg / ml stock solution in PBS, 90-100 μl) and incubated for 2 hours at 34° C.

Extraction

[0096] Postnatal day 4 Wistar rats were used for the study. Rats were placed in ice for 1 minute, the heads were decapitated and the cerebellum removed on ice. Cerebellum tissue was placed in 1 ml of 0.65% glucose supplemented PBS (10 μl 65% stock D (+)glucose / 1 ml PBS) in a large petri dish, chopped up into smaller sections and triturate with a 1 ml insulin syringe via a 23 G (0.4 mm) needle, and then squirted back into the glucose solution on the large petri dish. The tissue was sieved through (125 μm pore size gaze) and cent...

experiment 2

[0103] Effects of cPG after 6-OHDA induced nigral-striatal lesion.

Materials and Methods

[0104] Twenty male Wistar rats (280-310 g) were used. After exposing the skull, 6-OHDA (8 μg in a base of 2 μl 0.9% saline containing 1% ascorbic acid) was administered into the right medial forebrain bundle (MFB) using co-ordinates AP +4.7 mm, R 1.6 mmv-8 mm under 3% halothane anaesthesia. 6-OHDA was injected through a 25 G needle connected via a polyethylene catheter to a 100 μl Hamilton syringe. The 6-OHDA was infused by a microdialysis infusion pump at a rate of 0.5 μl / min. The needle was left in the brain for a further 3 minutes before being slowly withdrawn. The skin was sutured with 2.0 silk and the rats were allowed to recover from anaesthesia. The rats were housed in a holding room with free access to food and water at all times except during behavioural testing.

[0105] Cyclic PG was dissolved in saline. Four different doses of cPG (0, 0.1 0.5 1 mg / kg, Bachem) were administered intrape...

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Abstract

The invention relates to the use of cyclic Prolyl Glycine (“cyclic PG” or “cPG”) and analogs and mimetics thereof, as neuroprotective agents for the treatment and or prevention of neurological disorders including but not limited to cerebral ischemia or cerebral infarction resulting from a range of phenomena, such as thromboembolic or hemorrhagic stroke, cerebral basospasms, hypoglycemia, cardiac arrest, status epilepticus, perinatal asphyxia, anoxia such as from drowning, pulmonary surgery, and cerebral trauma, as well as to the treatment and prevention of chronic neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, and as anticonvulsants.

Description

CROSS-REFERENCE TO RELATED APPLICATIONS [0001] This application claims benefit of priority to New Zealand provisional patent No. 515432 filed Nov. 13, 2001, and U.S. provisional patent application Ser. No. 60 / 405,909 filed Aug. 26, 2002, and both incorporated by reference herein.BACKGROUND OF THE INVENTION NMDA AMPA Receptors [0002] Excessive excitation by neurotransmitters can cause the degeneration and death of neurons. It is believed that this degeneration is in part mediated by the excitotoxic actions of the excitotoxic amino acids (EAA) glutamate and aspartate at the N-methyl-D-aspartate (NMDA) receptor, the alpha-amino-3-hydroxy-5-methyl 4-isoxazole proprionic acid (AMPA) receptor, and the kainate receptor. AMPA / Kainate receptors may be referred to jointly as non-NMDA receptors. [0003] This excitotoxic action is considered responsible for the loss of neurons in cerebrovascular disorders such as cerebral ischemia or cerebral infarction resulting from a range of conditions, suc...

Claims

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Application Information

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Patent Type & Authority Applications(United States)
IPC IPC(8): A61K38/12A61P25/16A61P25/28A61K38/18A61K38/19A61K38/27A61K38/30
CPCA61K38/00A61K38/05A61K45/06A61P25/16A61P25/28
Inventor TRAN, LOI H.
Owner TRAN LOI H
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