Creatinol O-Phosphate (also known as Creatinolphosphate or Aplodan), sometimes abbreviated as COP, is a cardioprotective drug that appears to have been well researched a few decades ago and has since had a lack of recent studies.
The name of the molecular structure in full is N-methyl-N-(beta-hydroxyethyl)guanidine O-phosphate. The molecule of COP is different than that of the phosphorylated form of creatine, as the phosphate group is attached to a different segment of the creatine molecule. COP has not yet been shown to carry the traditional benefits of creatine supplementation, and for practical purposes should be seen as a different molecule.
Creatinol-O-Phosphate injections appear to be distributed in all tissues with most concentrated in the myocardium, liver, and kidneys; being excreted (as creatinol) when dephosphorylated.
100umol/L of COP can invoke a positive ionotropic effect that is glucose dependent and a slight negative chronotropic effect when oxygen is in the range of normoxia, and helped the recovery of cardiac contractility after ischemia (lack of oxygen) which is thought to be via a glycolytic mechanism.
One study that used isoprenaline (beta-adrenergic agonist) in a dose that was able to induce cardiac lesions noted that pretreatment of 200mg/kg COP (injections) was able to significantly attenuate the degree of cardiac lesions and doses up to 1000mg/kg have been shown to dose-dependently reduce death induced by an overdose of isoprenaline in mice (16% reduction at 250mg/kg, 50% reduction at 1000mg/kg). Low doses can increase in efficacy over 4 days of loading when compared to the same dose taken 4 hours acutely prior to the isoprenaline insult, and these effects may occur in a rehabilitative manner as evidence by 3060mg of Creatinol O-Phosphate given for three days (IV) to persons who recently suffered a Myocardial infarction, where serum cardiac enzymes decreased by 33-46% relative to control.
Injections of Creatinol O-Phosphate have an apparent cardioprotective effect against beta-adrenergic induced lesions and may possibly be rehabilitative as well; no studies on oral ingestion at this time
A reduction in the time required for atropine to induce cardiac arrythmia in guinea pigs has also been noted. Anti-arrythmic properties have been noted in vivo with COP supplementation even after three days of 2040mg (twice daily 1020mg injections).
Administration of COP, as well as the reference drug atropine, have been shown to improve A-V conduction of the heart in a small sample (n=6) pilot study; atropine's benefits were more evidence.
Injections of COP appear to be beneficial for arrythmia disturbances, no studies on oral ingestion
In rats, injections of up to 1000mg/kg appear to not be associated with death acutely
In otherwise healthy humans, intravenous doses of up to 3060mg COP failed to alter Arterial pressure, heart rate, ECG pattern, or all aspects aside from phosphorus levels (which increased following 2040-3060mg) in a blood panel; an increase in urinary phosphorus and diuresis also resulted with no overt signs of toxicity.
Currently appears to be safe following injections of up to around 3g, no studies conducted on oral administration