Description
TRO19622 (22033-87-0) is a neuroregenerative and neuroprotective agent acting at components of the mitochondrial permeability transition pore (MPTP).1Rescues motor neurons from axotomy-induced cell death and promotes nerve regeneration following sciatic nerve crush in mice. Reduces ROS and NLRP3 inflammasome activation in a mouse model of intracerebral hemorrhage.2Inhibits MPTP opening and protects neurons from apoptosis.3Induces oligodendrocyte maturation in culture and promotes myelin regenerationin vivoin a rodent model.4
Uses
TRO 19622 interacts with mitochondria proteins and is able to promote neuron survival under stress conditions. It is a potential drug for treating amyotrophic lateral sclerosis (ALS). TRO 19622 is a neuroregenerative and neuroprotective agent. This is a research product for neuroscience.
Uses
TRO 19622 has been used as a mitochondrial permeability transition pore inhibitor in mouse neurons
2. TRO 19622 is also known to stimulate myelin repair in rat models of demyelination
3.
Biological Activity
Neuroprotective and neuroregenerative compound. Rescues motor neurons from axotomy-induced cell death and promotes nerve regeneration following sciatic nerve crush in vivo . Binds directly to two components of the mitochondrial permeability pore, the voltage-dependent anion channel (VDAC) and translocator protein.
Biochem/physiol Actions
TRO 19622 can decrease axonal degradation and enhance the rescue of motor nerve conduction in peripheral neuropathy. Furthermore, TRO 19622 can reverse neuropathic pain and tactile allodynia in rat models of diabetes and chemotherapy-induced neuropathic pain4.
storage
Desiccate at +4°C
References
[1] THIERRY BORDET. Identification and characterization of cholest-4-en-3-one, oxime (TRO19622), a novel drug candidate for amyotrophic lateral sclerosis.[J]. ACS Applied Electronic Materials, 2007: 709-720. DOI:
10.1124/jpet.107.123000[2] QINGYI MA PHD Qin H M Sheng Chen MD, PHD John H Z M Hua Feng MD, PHD Jiping T M. NLRP3 inflammasome contributes to inflammation after intracerebral hemorrhage[J]. Annals of Neurology, 2013, 75 2: 209-219. DOI:
10.1002/ana.24070[3] LEE J MARTIN. The mitochondrial permeability transition pore regulates nitric oxide-mediated apoptosis of neurons induced by target deprivation.[J]. Journal of Neuroscience, 2011, 31 1: 359-370. DOI:
10.1523/jneurosci.2225-10.2011[4] K. MAGALON . Olesoxime favors oligodendrocyte differentiation through a functional interplay between mitochondria and microtubules[J]. Neuropharmacology, 2016, 111: Pages 293-303. DOI:
10.1016/j.neuropharm.2016.09.009
