IPH-AGAAПептид IPH-AGAA
About IPH-AGAA
Names in this research collection
IHP-AGAA
A research peptide evaluated in human-derived and rat muscle cultures. Marker expression is the endpoint.
Research background
A research peptide evaluated in human-derived and rat muscle cultures. Marker expression is the endpoint.
What the studies found
Lab research · 2017
Who or what was studiedHuman embryonic muscle-derived mesenchymal cells and rat primary muscle cultures.
Reported finding
Myogenic differentiation marker expression increased 2.9- and 2.8-fold at 20 and 200 ng/mL in human-derived cells.
- Myf5 marker
- 2.9- and 2.8-fold versus control20 and 200 ng/mL, respectively. The rat culture did not show the same differentiation response.
- p53 expression
- 1.6- and 1.5-fold lower20 and 200 ng/mL in human-derived cultures.
- Pax7 and Ki67
- About 1.2-fold changes at selected concentrationsMarker assays do not measure whole-muscle regeneration.
Methods, dose & source notes
Study of this preparation · International Journal of Applied and Fundamental Research, original report
Cell-culture results cannot establish a clinical dose or athletic benefit. Report alternates IPH and IHP spelling.
These highlights cover selected studies. Open a source for its methods, reported doses and full context.
- Compound class
- Experimental cell-culture peptide
- Research collection
- Actoprotection & occupational pharmacology · editorial grouping
- Research institutions
- No institutional affiliation recorded
- Source review
- Review dates and the material assessed are listed with each publication below.
Understanding the evidence
Human research
No human dosing study in the indexed source.
Study methods
Concentration-response cell marker experiments.
Independent replication
Independent replication is not established in the linked sources.
Source access
Original sources and the exact review scope are linked below.
Safety evidence
The linked experiments do not establish a safe human performance regimen.
Open a topic for the evidence assessment.
Linked sources
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