Neuroprotective Effects of ACTH4-10PRO8-GLY9-PRO10

NCT ID: NCT05648526

Last Updated: 2022-12-13

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

NA

Total Enrollment

42 participants

Study Classification

INTERVENTIONAL

Study Start Date

2021-08-01

Study Completion Date

2021-10-30

Brief Summary

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The compound ACTH4-10Pro8-Gly9-Pro10 is a synthetic analog molecule of an adrenocorticotropic hormone (ACTH) short fragment. That is free from hormonal effects and has neuromodulatory effects. We investigate the neuroprotective effects of ACTH4-10Pro8-Gly9-Pro10 can lessen neurotoxicity against ketamine in neonatal rats by looking at BDNF expression in the cortex and hippocampus tissue as well as BDNF blood levels.

Detailed Description

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The compound ACTH4-10Pro8-Gly9-Pro10 is a synthetic analog molecule of a short fragment of adrenocorticotropic hormone (ACTH). It is free from hormonal effects and has neuromodulatory effects. The immune-modulating and neurotrophic activity of the drug were shown to balance the state of anti-inflammatory and trophic factors (IL-IO, TNF-a, TGF-Pl, BDNF, NGF) over proinflammatory factors (IL-Ip, IL-8, CRP, LE) to increase the anti-apoptotic defense (Bcl-2 elevation), as well as to reduce the peroxidation process (increased SOD activity).

ACTH4-10Pro8-Gly9-Pro10 also has neuromodulator characteristics to function as a neuroprotector in inhibiting the apoptotic process. Modulation by ACTH4-10Pro8-Gly9-Pro10 will increase the levels of BDNF thereby inhibiting the process of apoptosis. Based on research by Gusev and Skvortsova, ischemic stroke patients who were given ACTH4-10Pro8-Gly9-Pro10 showed increased levels of BDNF, decreased mortality, and reduced length of stay. Based on the description above, the researcher was interested in analyzing the effect of the administration of ACTH4-10Pro8-Gly9-Pro10 on ketamine neurotoxicity in neonatal rats by assessing the level of BDNF.

Conditions

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Ketamine-Induced Neurotoxicity

Keywords

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ACTH4-10Pro8-Gly9-Pro10 BDNF ketamine-induced neurotoxicity apoptosis

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

PARALLEL

Primary Study Purpose

TREATMENT

Blinding Strategy

SINGLE

Investigators

Study Groups

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ACTH4-10PRO8-GLY9-PRO10

The compound ACTH4-10Pro8-Gly9-Pro10 is a synthetic analog molecule of a short fragment of adrenocorticotropic hormone (ACTH). It is free from hormonal effects and has neuromodulatory effects.

Group Type EXPERIMENTAL

ACTH4-10Pro8-Gly9-Pro10

Intervention Type DRUG

ACTH4-10Pro8-Gly9-Pro10 also has neuromodulator characteristics to function as a neuroprotector in inhibiting the apoptotic process. Modulation by ACTH4-10Pro8-Gly9-Pro10 will increase the levels of BDNF thereby inhibiting the process of apoptosis

ketamine 40 mg/kg BW subcutaneously

ketamine results in impaired brain function associated with neuroapoptosis injury in the immature brain.

Group Type ACTIVE_COMPARATOR

Ketamine

Intervention Type DRUG

negative-positive control (ketamine 40 mg/kg BW subcutaneously)

Interventions

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ACTH4-10Pro8-Gly9-Pro10

ACTH4-10Pro8-Gly9-Pro10 also has neuromodulator characteristics to function as a neuroprotector in inhibiting the apoptotic process. Modulation by ACTH4-10Pro8-Gly9-Pro10 will increase the levels of BDNF thereby inhibiting the process of apoptosis

Intervention Type DRUG

Ketamine

negative-positive control (ketamine 40 mg/kg BW subcutaneously)

Intervention Type DRUG

Eligibility Criteria

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Inclusion Criteria

* Rattus norvegicus rats
* Male, seven days old, weighing 15-20 grams
* Spraque-Dawley strain, obtained from the Experimental Animal Care Unit

Exclusion Criteria

* Animals that behave aggressively in observation by attacking other groups
Minimum Eligible Age

7 Days

Maximum Eligible Age

7 Days

Eligible Sex

MALE

Accepts Healthy Volunteers

No

Sponsors

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Universitas Sumatera Utara

OTHER

Sponsor Role lead

Responsible Party

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Raka Jati Prasetya

Doctor

Responsibility Role PRINCIPAL_INVESTIGATOR

Locations

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Faculty of Medicine Universitas Sumatera Utara

Medan, North Sumatra, Indonesia

Site Status

Countries

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Indonesia

References

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Ing C, DiMaggio C, Whitehouse A, Hegarty MK, Brady J, von Ungern-Sternberg BS, Davidson A, Wood AJ, Li G, Sun LS. Long-term differences in language and cognitive function after childhood exposure to anesthesia. Pediatrics. 2012 Sep;130(3):e476-85. doi: 10.1542/peds.2011-3822. Epub 2012 Aug 20.

Reference Type BACKGROUND
PMID: 22908104 (View on PubMed)

Flick RP, Katusic SK, Colligan RC, Wilder RT, Voigt RG, Olson MD, Sprung J, Weaver AL, Schroeder DR, Warner DO. Cognitive and behavioral outcomes after early exposure to anesthesia and surgery. Pediatrics. 2011 Nov;128(5):e1053-61. doi: 10.1542/peds.2011-0351. Epub 2011 Oct 3.

Reference Type RESULT
PMID: 21969289 (View on PubMed)

Other Identifiers

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Intervention

Identifier Type: -

Identifier Source: org_study_id