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Nilotinib Group Buy

nilotinib

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#391 Logic

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Posted 13 June 2016 - 06:24 PM

Round 2 quick progress report:

 

My apologies for neglecting this thread/everyone:

I am in the process of moving and my car died on me half way  to Durban! (coolant hose came adrift)

The package has reached the US and should be through customs and at the testing lab within the week.

 

 

 


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#392 Logic

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Posted 14 June 2016 - 09:48 AM

GoogleSiteSearch for lysosomes:

 

http://www.longecity...ndpost&p=506351

 

http://www.longecity...ndpost&p=714945

 

http://www.longecity...ndpost&p=622003

http://bmcbiol.biome.../1741-7007-9-38

 

http://www.longecity...ndpost&p=191792

...We demonstrate that oleuropein, the major constituent of Olea europea leaf extract, olive oil and olives, enhances the proteasome activities in vitro stronger than other known chemical activators...

 

http://www.longecity...ndpost&p=742045

...Finally, oleuropein aglycone-fed mice brain displayed an astonishingly intense autophagic reaction, as shown by the increase of autophagic markers expression and of lysosomal activity...

 

http://www.longecity...gy-anti-cancer/

 

http://www.longecity...ndpost&p=632285

 

I will get into this more when time allows.


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#393 Logic

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Posted 14 June 2016 - 01:55 PM

myelination:

 

http://www.longecity...te-myelination/

http://www.longecity...nerve-impulses/

http://www.longecity...ning-nootropic/

http://www.longecity...ncrease-myelin/

Methyl donors. The theory is that the immune system borrows methyl groups from choline to use as ammunition against invasion. Thus, when the nervous system begins to repair itself, the T Cells will look the oligodendrocites up and down, looking for reason to kill them, spot citrulline damage, and blow the oligodenrocites to pieces using their chemical warfare. Provide the methyl donors, and the immune system will shut fe thuck up.

 



#394 mlsirkis

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Posted 14 June 2016 - 02:15 PM

GENERAL POST:
Please, someone who has tried N, is it super bitter?
What does it taste like?.
Can this be taken under the tongue without burning?
Thanks.



#395 mlsirkis

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Posted 14 June 2016 - 02:17 PM

Has anyone tasted our N and confirmed it is tasteless like Tasigna?
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#396 ceridwen

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Posted 14 June 2016 - 06:21 PM

Yes
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#397 LongLife

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Posted 14 June 2016 - 07:41 PM

GoogleSiteSearch for lysosomes:

http://www.longecity...ndpost&p=506351

 

http://www.longecity...ndpost&p=714945

 

http://www.longecity...ndpost&p=622003

 

http://bmcbiol.biome.../1741-7007-9-38

 

http://www.longecity...ndpost&p=191792

...We demonstrate that oleuropein, the major constituent of Olea europea leaf extract, olive oil and olives, enhances the proteasome activities in vitro stronger than other known chemical activators...

 

http://www.longecity...ndpost&p=742045

...Finally, oleuropein aglycone-fed mice brain displayed an astonishingly intense autophagic reaction, as shown by the increase of autophagic markers expression and of lysosomal activity...

 

http://www.longecity...gy-anti-cancer/

 

http://www.longecity...ndpost&p=632285

 

I will get into this more when time allows.

GENERAL INFORMATION:

In relation to the subject matter; Nilotinib's actions on Parkinson disorder symptoms.

 

What actions are these? Most are unknown and only recently some have been observed. Such as the "ability to cause" certain proteins (ie, misfolded problematic/fatal proteins; a-Synuclein, b-Amyloid, Tau, etc.) to degrade, disassociate and be recycled and/or removed from the body. These misfolded proteins, through yet unknown specific pathways, become insoluble, rigid, disorderly and attracted to themselves resulting in their contribution to some grave disorders such as Alzheimer's, Parkinson, Multiple Syndrome Atrophy (MSA), various Sclerosis's and others.

 

The "ability to cause" actions interests us, such as programmed cell death:

Apoptosis (Type I cell-death), Autophagy (Type II cell death); forms of programmed cell death [compared to Necrosis; a non-physiological process of cell death, caused by external factors, resulting from infection, trauma or injury or Pyroptosisa highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens.].

 
Where does Autophagy occur in the cell (humans) ?
Summary: the degradation of organelles [one of several structures with specialized functions, suspended in the cytoplasm of a eukaryotic -human in this case- cells] and long-lived proteins in the lysosome occurs by the process of autophagy, while misfolded and short-lived proteins are degraded in proteasomes located in the nucleus and in the cytoplasm [a protoplasm or the material within a living cell, excluding the nucleus].
 
So autophagy, a form of programmed cell death, occurs in humans inside the lysosome of each cell. Specifically the organelles and long lived proteins in the lysosome.
 
Lysosomes are a cellular organelle that contain acid hydrolase enzymes (Caspases); breaks down waste materials and cellular debris. Described as the "stomach of the cell", Lysosomes digest excess or worn-out organelles, food particles, and engulfed viruses or bacteria.
 
What are Caspases?
A family of specific enzymes that performs proteolysis; breaks down proteins and peptides (<40 amino acids) called protease enzymes, playing essential roles in programmed cell death (including apoptosis, pyroptosis and necroptosis) and inflammation. 
Cysteine-Aspartic proteases, 
Cysteine Aspartases or,
Cysteine-dependent Aspartate
enzymes that performs proteolysis
 
Human cellular Autophagy happens in Lysosomes via Caspase (simplified version). Our defense against neurodegeneration, as well as other disorders, depends on our lysosomes to a great degree
 

We know that autophagy is induced by Silent Information Regulators (SIR) protein/genes or Sirtuin's (ie, Sirt1; caspase-1-sirtuin 1 pathway example) because they are thought to contribute to regulation of fat storage, low blood cholesterol, low blood glucose levels, and low insulin levels. Sirtuins's regulation of these important health indicators is assumed to be an important part of the explanation for why Caloric Restriction [CR] increases lifespan.

 

Therefore CR mimicking brought about through Sirt1 and Sirt3 is an action call for inducing Autophagy, cellular cannibalism. It could be said that Sirt1 and Sirt3 (as well as other substances) stimulates lysosomes to Autophagy.

 

There are polyphenolic activators of Sirtuins, natural products such as resveratrol, butein and piceatannol as well as altered products like pterostilbene.

 

I hope that reviewing this general information may help some of us better comprehend some of the articles posted above by LOGIC, whom again has done a very good job of hunting out relevant material.


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#398 resveratrol_guy

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Posted 15 June 2016 - 02:53 AM

Has anyone tasted our N and confirmed it is tasteless like Tasigna?

 

It sounds like it does not, based on the above. I suppose we could send some to Park2009 and have him compare. But it ultimately doesn't matter much. What we need to determine is whether it works or not. I would hate to discard this stuff due to some inconsequential difference between the two. Bitterness sounds to me like a good thing, all else being equal, because anticancer substances in fruits and veggies tend to taste bitter on account of the OH groups in the active molecules. If this stuff were fake, I would expect it to taste acidic (because grain powders would be the cheapest way to fake it) or like toxic solvents (on account of the VOCs in various paints and dyes).

 

Glad you're OK, Logic.



#399 LongLife

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Posted 15 June 2016 - 03:32 AM

Yes

CERIDWEN:

 "YES" meaning...it does taste like the commercial form of [N]? Or "YES" for something else? Help me out understanding your comment please. Thanks:-)



#400 Mian Ali Ismail

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Posted 15 June 2016 - 10:17 AM

This artcle seems to describe the condition of the patient in more detail.What is interesting is the patient was able to walk who was bedridden earlier.

 

A remarkable study was published about the treatment of a 77-year-old Caucasian man with severe dementia and behavioral disturbance. The man was admitted with late onset Alzheimer’s Disease and treated with memamtine. His condition however continued to decline. 16 months after the start of memamtine treatment the patient’s condition had severely worsened. He was unable to remember his name, the calendar date, day of the week, year, or place, and could not recognize family members. Additional impairments included slurred speech, expressive aphasia, loss of bowel/bladder control, and lack of coordination marked by an inability to sit, stand, or walk unassisted.

At that point the family gave the researchers consent to start an experimental treatment with human recombinant deoxyribonuclease I (DNase I) (1500 KU/mg) given orally three times a day in conjunction with his continued memantine therapy. The DNase I was well tolerated, and no averse or unanticipated events were registered.

The reseachers reported the following results:
Our patient demonstrated considerable cognitive improvement beginning on the second day of DNase I treatment, becoming partially oriented to time and place, and once again recognizing and remembering the names of family members. He further became able to dress himself, including tying shoelaces and buttons, as well as walk independently, feed himself, and use an exercise bike. Neurologic abnormalities affecting his gait were significantly reduced. His MMSE score increased dramatically from 3 to 16, and his FAST score was reduced from 7 to 5. However, he continued to score low on the MMSE for measures of orientation to time and place, memory, and visuospatial construction.

Two months following the initiation of DNase I treatment (19 months following initiation of memantine treatment), our patient exhibited an MMSE score 18 and a FAST score of 4. Moderate improvements in memory were observed, although visuospatial construction continued to decline. He was better able to speak and interact with others, recognize relatives, and actively attend to television programs. Our patient further became able to perform calculations, play piano, chess, and walk independently.

DNase I, is an endonuclease coded by the human gene DNASE1. DNase I is a nuclease (an enzyme that cleaves the chains of nucleotides into smaller units) that cleaves DNA. It acts on single-stranded DNA, double-stranded DNA, and chromatin. In addition to its role as a waste-management endonuclease, it has been suggested to be one of the deoxyribonucleases responsible for DNA fragmentation during apoptosis.

Cell-free DNA (cf-DNA), including bacteria-derived DNA, may be another target. The researchers noted that circulating cf-DNA has been observed to play an important role in the progression and maintenance of different disease states, including cancer, stroke, and other.

In addition, it has been suggested that cf-DNA could promote auto-inflammation. In this study which was published by another group of researchers at roughly the same time auto-inflammation was observed to be a possible cause of dementia. The researchers put together strong arguments that the neurological decline common to these diseases is caused by ‘auto-inflammation’, where the body’s own immune system develops a persistent inflammatory response and causes brain cells to die.

Another positive aspect is that the use of DNase I for the treatment of a disease called cystic fibrosis was approved on December 30, 1993 by the Food and Drug Administration (FDA) which means it is commonly available today. It is also a good example of strengthening the abilities of the own body to treat diseases. In this case 40 mg of human recombinant DNase I (1500 KU/mg) was given orally three times a day in conjunction with the memantine therapy (10 mg daily). The DNase I was well tolerated, and no averse or unanticipated events were registered.

Ofcourse further research is required but the results sound so spectacular that it may make sense to inquire with treating physicians of loved ones that are in a late/terminal stage of dementia about the possibilities to repeat the treatment carried out in this study.


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#401 Mian Ali Ismail

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Posted 15 June 2016 - 10:24 AM

Thnks guies for showing interest.Im currently in talk with Logic to arrange a group buy for Dnase 1 who will contract the suppliers ! I will let you guies know of any recent development.


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#402 Mian Ali Ismail

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Posted 20 June 2016 - 08:05 PM

 Is anybody already taking Dnase 1 and can pulmozyme used in nebulizer be taken orally without any sideeffects ?



#403 LongLife

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Posted 20 June 2016 - 09:16 PM

Thnks guies for showing interest.Im currently in talk with Logic to arrange a group buy for Dnase 1 who will contract the suppliers ! I will let you guies know of any recent development.

MIAN ALI ISMAIL & LOGIC:

 

I'm in on a Group Buy of Dnase1 (Deoxyribonuclease I), let's get a threat going on this right way.


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#404 Logic

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Posted 21 June 2016 - 08:44 AM

Round 2 quick progress report:
 
The N was at customs for a worryingly long time, but is now in the US and on its way to the testing lab.

 

Fedex says this is normal, with some packages/consignments taking longer than others to clear customs for numerous reasons, such as a large volume of work/imports at the time of the package's arrival.

They apologised for the delay, as do I.  I hope to have the test results posted soon.

 

 


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#405 Logic

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Posted 23 June 2016 - 08:04 AM

Round 2 progress report:

 

The N is at the testing lab.

I will confirm with them when its 8am there.

This means that my predictions should now be more reliable and that the N should be posted to all the end users next week. 

 

 


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#406 Mian Ali Ismail

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Posted 24 June 2016 - 04:04 AM

Treatment with DNase I in the present case allowed our patient to withdraw from a terminal state and resulted in significant improvements in cognitive and behavioral function, including the ability to walk and perform everyday tasks with near independence. DNase I was used as a repurposed FDA-approved medication [14]. Significant recovery was observed in all areas of cognitive and motor function, indicating the possibility of a DNase-sensitive target involved in generating the symptoms of AD.

Cell-free DNA, including bacteria-derived DNA, may be one such target [15]. Circulating cf-DNA has been observed to play an important role in the progression and maintenance of different disease states, including cancer, stroke, and other [1617]. Our previous research revealed its possible role as a therapeutic target in graft-versus-host diseases [18].

Though there are various suggestions regarding the origins of serum and plasma cf-DNA, many researchers have speculated that it results from apoptosis, necrosis, or both, or that this cf-DNA is secreted by cancer cells, microorganisms, hematopoietic cells, and/or neutrophils [19]. However, the physiological role of cf-DNA in the progression of these diseases remains to be discovered. Some have theorized that this role is mechanical in nature, increasing blood viscosity and leading to ischemia, while others suggest that cellular uptake of cf-DNA is involved in the development of metastatic conditions [20]. Little research has focused on the role of cf-DNA in neurodegenerative conditions, particularly AD. Further studies are required in order to evaluate the role of cf-DNA in the incidence and progression of neurodegenerative pathologies.


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#407 Logic

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Posted 24 June 2016 - 02:07 PM

 

Thnks guies for showing interest.Im currently in talk with Logic to arrange a group buy for Dnase 1 who will contract the suppliers ! I will let you guies know of any recent development.

MIAN ALI ISMAIL & LOGIC:

 

I'm in on a Group Buy of Dnase1 (Deoxyribonuclease I), let's get a threat going on this right way.

 

 

Thread is here:

http://www.longecity...nt-with-dnase1/



#408 Linda Gray

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Posted 26 June 2016 - 12:56 PM

Have there been any reports of improvements from the first N group buy?
Have there been any reports of improvements from the first N group buy?

#409 LongLife

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Posted 26 June 2016 - 02:51 PM

Have there been any reports of improvements from the first N group buy?
Have there been any reports of improvements from the first N group buy?

Greetings. Too soon right now. No bad news, which is good news. A follow-up is underway and we will shoot for Friday, July 8th as an update day on progress; comments and observations. 



#410 KieranA001

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Posted 26 June 2016 - 06:58 PM

Am very intrested in buying some. Are you going to do another group buy or can I still buy some? :) My memory and visual / cognitive function is getting worse and worse. I've heard Centrophenoxine helps as well, due to its ability to clear b-amyloid proteins. Maybe try a combo, don't know how safe that would be though. :/ 



#411 MarcB

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Posted 28 June 2016 - 05:10 PM

Has anyone else reviewed these?  Pretty compelling.

 

https://www.youtube....h?v=QUTzY5c6JOg

 

https://www.youtube....h?v=MoD37BbVeNM

 

91/2 mins.  This link is just the PD patient

 

https://www.youtube....h?v=oGTkwaZoabs

 

4 ½ minutes

https://www.youtube....h?v=YnVI-nPYkNk

 

4 mins, more neurological basis for TMJ treatment for Parkinson's diagnosis

https://www.youtube....h?v=cXVR423Xlpc


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#412 45rpm

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Posted 30 June 2016 - 06:24 AM

Like most of the people on this board, I have been aware of Turmeric/Curcumin as a potential treatment for Parkinson's Disease. I've tried it on my mother in the past but with no success. Although there seems to be much interest in the spice, I didn't view it as a good candidate for treating the disease.

 

Then imagine my surprise when I found this article about a derivative of Curcumin, which has some interesting properties including the ability to dissolve amyloid plaques and to extend lifespans. The substance is called J147. It was discovered in 2012 and I've never heard of it before. Does anyone have any experience with this?

 

http://www.alzheimer...ricept-for.html

http://www.ncbi.nlm....pubmed/23673233

 

Supplier of J147

https://www.tocris.c...p?ItemId=399926

 

 

Here's some more information about J147:

 

"Beginning with curcumin, a compound extracted from the spice turmeric (associated with aiding the healing process), they found that a heterocyclic derivative of curcumin showed significant neuroprotective abilities in the various neuron cultures.  A large number of derivatives were formed in a single reaction having multiple end points.  These products were then separated and tested individually.  J147 was the most promising candidate product of this process.

 

If you sat down to design an Alzheimer’s drug candidate, you couldn’t get much better than J147.  It is reasonably small (molecular weight of 351), penetrates the blood-brain barrier, is orally active, and appears to have no obvious side effects.  It is strongly neuroprotective, with broad activity at levels many times greater than the compounds from which it was developed.  It has brain-derived neurotrophic factor-like effects without requiring the presence of the BDNF receptor. 

 

In tests with healthy rats and mice, J147 is found to enhance both short- and long-term memory following a short period of treatment.  In Alzheimer’s rats and mice, learning was enhanced, and short-term memory deficits were reversed with short-term treatment.  J147 reduces oxidative stress and the associated damage from immune reaction and free-radicals.

 

J147 also increases the expression of BDNF without requiring BDNF receptors, apparently by activating downstream targets of BDNF.  This activity supports long-term memory and the survival of existing neurons, as well as the growth and differentiation of new neurons and synaptic structures.  BDNF receptors are primarily located in the hippocampus, cortex and basal forebrain, but the BDNF-like activity of J147 may be felt in other parts of the brain, offering possible treatments for depression and similar disorders."

 

SOURCE:

https://www.patexia....e-research-1823


Edited by 45rpm, 30 June 2016 - 06:30 AM.


#413 45rpm

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Posted 30 June 2016 - 07:54 AM

I apologize but I hadn't realized that there's at least two existing threads on LongeCity concerning J147...

 

http://www.longecity...min-derivative/

http://www.longecity...rcumin-extract/



#414 Logic

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Posted 30 June 2016 - 09:32 AM

Phase II trial of N for PD:
https://gumc.georget.../2016/parkinson


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#415 centralFloridaMan

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Posted 01 July 2016 - 12:53 AM

hi,  With all of the excitement about nilotinib et al.  I thought you might be interested in a phase 1 clinical trial by Prothena with Roche.  It uses monoclonal antibodies to clean alpha synuclein from the brain.  I am aware of this because Compass Research in Orlando, Fl was enlisting volunteers for the study and i was rejected because of an issue with my brain scan.  Prothena has released positive results in what i would call a careful manner.  However, my neurologist is the principal investigator for the orlando part of the study and he has indicated that the 96% reduction in alpha synuclein that they saw after one treatment not only reduced alpha synuclein but had as they thought it would, pretty dramatic results with patients improving very significantly very quickly.  My neuro has indicated that i can get into phase 11 so i am pretty excited about this.  Incidentally the kind of positive therapeutic results they saw in phase 1 are not typical.  There are apparently several studies around the country and in europe with ongoing clinical trials of monoclonal antibodies some in phase 11 already.  

 

ir.prothena.com/releasedetail.cfm?releaseid=902569
  1.  
  2.  

 


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#416 Ark

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Posted 01 July 2016 - 01:33 AM

https://www.google.c..._Y6TxMkzs_ASQrg

#417 David Watford

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Posted 04 July 2016 - 09:36 PM

Group Buy No 2

Now that this delivery is nigh, I'd find it helpful to gather from those in Group Buy 1 as to how they prepared and measured their daily doses (e.g. did they make capsules).

 

The thought also arose that we might be able to make this purchase into a legitimate trial.  The trial may not be that rigorous, but may be able to help the PD community by providing valuable information to other researchers who are unable to take the risks that we are prepared to take. My neurologist is quite keen to monitor my own progress (while, understandably, not taking responsibility) by carrying out a baseline assessment and then retesting on a monthly basis. Other doctors may be prepared to do the same.


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#418 Logic

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Posted 05 July 2016 - 12:52 AM

 

Nilotinib Attenuates Renal Injury and Prolongs Survival in Chronic Kidney Disease

 

...We administered either nilotinib or vehicle to Sprague–Dawley rats beginning 2 weeks after 5/6 nephrectomy (Nx) or laparotomy and continuing for 8 weeks. Serum creatinine levels were significantly lower in the nilotinib group after 6 and 8 weeks of treatment. Furthermore, nilotinib-treated rats had less proteinuria, attenuated glomerulosclerosis and tubulointerstitial damage, and reduced macrophage infiltration into the tubulointerstitium...nilotinib treatment significantly prolonged survival. Taken together, these results suggest that nilotinib may limit the progression of chronic kidney disease...


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#419 Logjam

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Posted 05 July 2016 - 01:26 AM

Proposed reason/mechanism:  The effects may be mediated by inactivation of PDGFRs and inhibition of macrophage accumulation and subsequent cytokine production, resulting in less vigorous fibrotic and inflammatory responses.

 

PDGFR = https://en.wikipedia...factor_receptor

 

I posted something about neurological disease and DYRK1A (inhibition) if anyone is interested, but don't want to sidetrack the thread.  It's interesting that one of the DYRK1A inhibitors was used early on for Parkinsons.  See http://www.longecity...downs-diabetes/

 

 

 

 

Nilotinib Attenuates Renal Injury and Prolongs Survival in Chronic Kidney Disease

 

...We administered either nilotinib or vehicle to Sprague–Dawley rats beginning 2 weeks after 5/6 nephrectomy (Nx) or laparotomy and continuing for 8 weeks. Serum creatinine levels were significantly lower in the nilotinib group after 6 and 8 weeks of treatment. Furthermore, nilotinib-treated rats had less proteinuria, attenuated glomerulosclerosis and tubulointerstitial damage, and reduced macrophage infiltration into the tubulointerstitium...nilotinib treatment significantly prolonged survival. Taken together, these results suggest that nilotinib may limit the progression of chronic kidney disease...

 

 


Edited by Logjam, 05 July 2016 - 01:27 AM.

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#420 Logic

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Posted 07 July 2016 - 03:20 PM

Round 2 progress report:

 

The lab has:

"...Finished the this [testing] earlier today: Looks very, very similar to the last batch...I'll start weighing and packing in the afternoon..."

 

I will post the test results as soon as I have them.
 


Edited by Logic, 07 July 2016 - 03:20 PM.






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