Seems like a long time to extend testing on already approved drugs if trials are positive. In the case of Nilotinib doses are much lower for PD patients. Not sure what hoops have to be jumped through to fast tract these approved drugs. First at least in the case of Nilotinib we have to wait for official published results and hope they compare to the unofficial results I was told. And I agree with ST that a lot can go wrong especially, in this case , the funding. STill I'm staying upbeat about this drug. I have to believe something out there is going to work for us to keep me going.
All the best to everyone.

It does seem like a long time. I was just comparing it to the FDA requirements for the more advanced trial of Isradipine, which is also approve; has been on the market much longer; and as a hypertension drug, is much safer than nilotinib, which is a chemotherapy drug.

I asked about side effects associated with Nilotinib the first time this trial was mentioned to me. As soon as I heard it was a chemo drug I asked about hair loss. I was told that this drug doesn't kill cells it "mops up or cleans" up cells so hair loss shouldn't be a problem especially at the lower doses given during this trial. The neurologist told me they have about a 1% patient population experiencing hair loss. During the current trial when I asked about side effects I was told that in the 10 patients the main side effect they were seeing was agitation which occurs when too much dopamine is on board. This lead to a reduction in Parkinson medications in the affected patients. I just hope all this continues over the next three months and the official published report is as encouraging as this unofficial report.
This is the only encouraging news I've heard lately concerning this disease and what is keeping me going. Just wanted to share some good news with everyone I'm as desperate as the next person for a cure or at the least stopping disease progression. We can all just hope and pray the end official report is as encouraging as the unofficial report I've been given. So far so good.
All the best to everyone.

Mechanism of Nilotinib (animal study)
 

Use of Nilotinib Cancer Drug for Treatment of Parkinson’s, Alzheimer’s, Dementia

Hum. Mol. Genet. (2013)doi: 10.1093/hmg/ddt192 First published online: May 10, 2013

Nilotinib reverses loss of dopamine neurons and improves motor behavior via autophagic degradation of α-synuclein in Parkinson’s disease models

Michaeline L. Hebron†, Irina Lonskaya† and Charbel E.-H. Moussa
Abstract

Parkinson’s disease is a movement disorder characterized by death of dopaminergic substantia nigra (SN) neurons and brain accumulation of α-synuclein. The tyrosine kinase Abl is activated in neurodegeneration.Here, we show that lentiviral expression of α-synuclein in the mouse SN leads to Abl activation (phosphorylation) and lentiviral Abl expression increases α-synuclein levels, in agreement with Abl activation in PD brains.

Administration of the tyrosine kinase inhibitor nilotinib decreases Abl activity and ameliorates autophagic clearance of α-synuclein in transgenic and lentiviral gene transfer models. Subcellular fractionation shows accumulation of α-synuclein and hyper-phosphorylated Tau (p-Tau) in autophagic vacuoles in α-synuclein expressing brains, but nilotinib enhances protein deposition into the lysosomes.

Nilotinib is used for adult leukemia treatment and it enters the brain within US Food and Drug Administration approved doses, leading to autophagic degradation of α-synuclein, protection of SN neurons and amelioration of motor performance.

These data suggest that nilotinib may be a therapeutic strategy to degrade α-synuclein in PD and other α-synucleinopathies.
[Show]
Citation

Girija mentions tyrosine kinase inhibitors.

If we assume that:
- tyrosine kinase inhibitors are an effective treatment for PD.
- any commercial drugs will take at least five years to get to market and even then be too expensive for many.

Then it make sense to see if there are any natural substances with this property.

A quick Google gives:

- curcumin;

- genistein (found in broad (fava) beans, soybeans, coffee, kudzu).

Rick mentioned genistein back in 2012:
http://neurotalk.psychcentral.com/sh...ight=genistein

A quick sanity check:

- epidemiological results suggest that coffee consumption is negatively associated with PD.

- genistein crosses the BBB.

John

Further tyrosine kinase inhibitors activate AMPK which initiates autophagy so
gynostemma tea should help PWP!

As researchers continue to unravel the mysteries of AMPK, they have discovered four ways to boost the body’s AMPK activity:

Exercise: AMPK activity increases with regular vigorous exercise.73 This beneficial effect of exercise on AMPK, however, may vanish in the elderly.5
Calorie Restriction: When you under eat, you create increased AMPK activity as cells sense a requirement to function more efficiently in the presence of diminished energy (food) intake. However, when normal food intake resumes, AMPK activity declines.74,75
Metformin: One of the drug metformin’s most beneficial mechanisms is to activate AMPK.76 This is one way it lowers elevated glucose.77 Unfortunately, most physicians only prescribe metformin for type II diabetes, making access to this drug difficult for most people. Some people also experience digestive upset in response to metformin and cannot take it.78
Botanical Extracts: Two natural agents (the Chinese herb Gynostemma pentaphyllum79 and trans -tiliroside derived from rose hips80) have been shown to activate AMPK. Each of these agents triggers different downstream metabolic benefits, and in one study, trans-tiliroside led to an even greater glucose-lowering effect than the AMPK-activating antidiabetic drug metformin.81

With these four documented methods of boosting AMPK signaling, there is no reason for aging humans to suffer the degenerative impact caused by loss of activated AMPK.

As Gynostemma is a blood thinner be sure to talk with your MD before taking this herb.

http://www.lef.org/Magazine/2014/SS/AMPK/Page-01?p=1

Nilotinib and Parkinson
 

Since the formal report was released in Oct. 2015, the result was promising.

How about the Nilotinib tiral ii ? Does anyone kindly konw?

sami, I saw the brief abstract released at the Neuroscience conference in Chicago last Oct. However, I haven't yet seen the full report. Do you have a link to an actual published report?

I have an appointment at Georgetown Medstar UH, January 20. I'll ask about the trial but my neurologist isn't working directly with the trial and couldn't give me much information at my last visit the end of October. The doctor that was seeing me and working directly with the trial has left Georgetown and is now at the NIH. She was at GT on a fellowship. So I've lost my inside source but will see what, if anything I can find out this next appointment.

Phase ll Nilotinib Trial
 

My last appointment at Georgetown Medstar movement disorder clinic I got some Information about the second phase of the Nilotinib trial. It's scheduled to start this summer and has funding. The funding is coming from foundations not Novartis. However Novartis is being approached to give the medications used in the trial. At the present time the trial will be testing the drug on stage l and stage ll PDers. It involves a lot of planning so my neuro said it could be delayed but he emphasized the funding was there. I don't know anything about the placebo group and how that will be handled. I go back again in March and he said he would give me all the current information he has on the trial at that time.
This is all I have at this time but will keep you posted about any information I'm told at my appointments. I'll ask about the placebo groups next visit.