Everything about Mibolerone(Cheque drops)
|1.What is IDFP(615250-02-7)|
| 2.How does IDFP(615250-02-7)works? |
| 3.IDFP(615250-02-7) effects |
| 4.IDFP(615250-02-7) dosage |
| 5. IDFP(615250-02-7) warning |
| 6.IDFP(615250-02-7) reviews |
I.IDFP basic Characters:
IDFP(615250-02-7), is an organophosphorus compound related to the nerve agent sarin. Chemical name include: IDFP;ISOPROPYL DODECYLFLUOROPHOSPHONATE;P-DODECYL-1-METHYLETHYL ESTER-PHOSPHONOFLUORIDIC ACID;1-[fluoro(propan-2-yloxy)phosphoryl]dodecane.
|Decription||IDFP is an organophosphorus compound related to the nerve agent sarin. Like sarin, IDFP is an irreversible inhibitor for a number of different enzymes that normally serve to break down neurotransmitters|
The endocannabinoids, 2-arachidonoyl glycerol (2-AG) and arachidonoyl ethanolamide (AEA), are biologically active lipids that regulate diverse neurological and metabolic functions by activating the cannabinoid receptors, central cannabinoid (CB1) and peripheral cannabinoid (CB2). Monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH) hydrolyze 2-AG and AEA, respectively, thus terminating their biological function. IDFP (615250-02-7)is an organophosphorus compound that dually inhibits MAGL and FAAH with IC50 values of 0.8 and 3 nM, respectively.1 At 10 mg/kg, IDFP elevates brain levels of 2-AG and AEA more than 10-fold, and decreases levels of arachidonic acid by a similar magnitude.
CB1-dependent cannabinoid behavioral effects
What are IDFP(615250-02-7)effects? Within 5 min after treatment with IDFP (10 mg kg−1, i.p.), mice adopted a flattened posture and remained motionless with their eyes open. This state of immobility was qualitatively reminiscent of behavioral responses elicited by direct CB1 agonists, which motivated us to examine IDFP-treated animals in the tetrad tests for cannabinoid behaviors. IDFP was found to produce all four behavioral effects expected from stimulating CB1-hypomotility, analgesia, catalepsy and hypothermia. These behavioral effects were blocked by pretreatment with the CB1 receptor antagonist AM25120 and were absent in CB1(−/−) mice21 . These results suggested that blockade of endocannabinoid metabolism was responsible for the observed action of IDFP effects. The magnitude of effects observed with IDFP was similar to that with a direct CB1 agonist, WIN55212-2 (10 mg kg−1, i.p.). Using similar mouse brain membrane preparations, IDFP displaces CB1 agonist binding in vitro with an IC50 of 2 nM17, similar to its IC50 for MAGL (0.8 nM) and FAAH (3 nM) , whereas even at 30 nM it did not significantly (5 ± 9 %, n=6, p>0.05) stimulate guanosine triphosphate binding. This suggests IDFP effects is not acting as a direct receptor agonist at relevant concentrations.
Disruption of endocannabinoid metabolism in vivo
Endocannabinoid-hydrolyzing activities were examined in brain extracts from IDFP- (10 mg kg−1, i.p.) and vehicle-treated mice. This treatment level for IDFP was chosen from dose-response relationships for producing cannabinoid-like behavior. Four h post-treatment, hydrolysis of 2-AG and anandamide was inhibited by 86 ± 1 % and 94 ± 1 %, respectively, in brain tissue from IDFP-treated animals. In contrast, no detectable inhibition of AChE was observed with IDFP in the same experiment, consistent with the absence of cholinergic toxicity. IDFP is a long chain analog of sarin with dodecyl replacing methyl, a change resulting in low AChE inhibitory potency.
The reduced levels of endocannabinoid hydrolytic activity observed in brain tissue of IDFP-treated animals correlated with more than 10-fold increases in brain levels of both 2-AG and anandamide. Several other changes in brain lipid chemistry were also observed in IDFP–treated animals, including elevations in additional N-acylethanolamines (NAEs) [e.g., N-palmitoyl- and N-oleoylethanolamines and monoacylglycerols [2-and 1-palmitoylglycerol and 2- and 1-oleoylglycerol]. Interestingly, AA levels were decreased by IDFP in amounts equivalent to the elevations detected for 2-AG. These data establish that IDFP is a potent blocker of 2-AG and anandamide metabolism in vivo, leading to highly elevated brain levels of both endocannabinoids and a concurrent decrease in free AA levels.
For long term storage,we suggest that IDFP dosage be stored as supplied at -20℃. It should be stable for at least one year.
IDFP is supplied as solution in methyl acetate. To change the solvent,simply evaporate the methyl acetate under a gentle stream of nitrogenand immediately add the solvent of choice.Solvents such as ethanol,DMSO,and dimethyl formamide purged with an inert gas can be used. The solubility of IDFP in these solvents is approximately 10mg/ml.
If aqueous stock solutions are required for biological experiments,they can best be prepared by diluting the organic solvent into aqueous buffers or isotonic saline.Ensure that the residual amount of organicsolvent is insignificant,since organic solvents may have physiological effects at low concentrations.We do not recommend storingthe aqueous solution for more than one day.
IDFP(615250-02-7) is not for human or veterinary use，more warning is still in researching. Avoid direct contact with skin, eyes, respiratory tract, any discomfort, call your doctor right away.
IDFP(615250-02-7) is an organophosphorus compound related to the nerve agent sarin. Like sarin, IDFP is an irreversible inhibitor for a number of different enzymes that normally serve to break down neurotransmitters, however the long alkyl chain of IDFP makes it dramatically weaker as an inhibitor of acetylcholinesterase (AChE), with an IC50 of only 6300nM, while it is a potent inhibitor of two enzymes monoacylglycerol lipase (MAGL), the primary enzyme responsible for degrading the endocannabinoid 2-arachidonoylglycerol (2-AG), and fatty acid amide hydrolase (FAAH), the primary enzyme that degrades the other main endocannabinoid anandamide. The IC50 of IDFP is 0.8nM at MAGL, and 3.0nM at FAAH. Inhibition of these two enzymes causes markedly increased levels of both anandamide and 2-AG in the brain, resulting in increased cannabinoid signalling and typical cannabinoid behavioral effects in animal studies, while its lack of potency at AChE means that no cholinergic symptoms are produced.Despite its similar chemical structure to the banned nerve agents, the long alkyl chain of IDFP causes it to fall outside the definition of “toxic chemicals” under the Chemical Weapons Convention,and since it also does not exhibit the potent AChE inhibition of related organophosphorus compounds, IDFP(615250-02-7) reviews is not subject to the same stringent legal controls.