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Questions Answered by Dr. Naviaux

Discussion in 'General ME/CFS News' started by RL_sparky, Sep 13, 2017.

  1. Murph

    Murph :)

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  2. RL_sparky

    RL_sparky Senior Member

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    Thanks for letting me know. I'll delete it and deal with it tomorrow some time!
     
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  3. RL_sparky

    RL_sparky Senior Member

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    The Revised Edition:

    Dr. Naviaux -- Questions September 13, 2017

    Questions regarding study design:
    1. Preliminary results presented by Ron Davis suggest that Suramin only partially turns off the disease process (as determined using nano-needle?). Is this the case?If so, is it worth pursuing a clinical trial with this drug and why?
    a. There are several layers to this question. 1st: None of the symptoms of ME/CFS, or any of the other non-monogenic, complex chronic diseases (eg, MS,ALS, PTSD, OCD, Parkinson, Alzheimer, Diabetes, IBD, Crohn’s, cancer, hypertension, heart disease, and dozens more) are the result of a single-cell problemthat can be studied in a dish. They are all the result of the communication failures between many cell types in many parts of the body. There is no way to testfor example, brain fog in a dish, or post-exertional malaise, non-restorative sleep, migraine headaches, fibromyalgia, microbiome dysbiosis, hypothalamic,pituitary, adrenal or thyroid dysfuntion, or postural orthostatic tachycardia syndrome (POTS) in a dish.
    b. 2nd: What Dr. Davis actually finds is that it is the plasma of patients with ME/CFS that causes the abnormalities he sees. Even cells from healthy controlsreact abnormally in his microfluidics impedance device when they are exposed to plasma from an ME/CFS patient.
    c. 3rd: There has never been a drug that has worked in a complex disease like ME/CFS, ie, succeeded in Phase I, II, and III clinical trials, that was discoveredby screening in a dish or a plate. While the cellular impedance abnormalities that Dr. Davis has found in some patients with ME/CFS may eventually help with“diagnosis”, they cannot be used to predict how a drug will work of actual symptoms like pain, fatigue, sleep, brain fog, hormone abnormalities, or autonomicnervous symptom problems.
    i. In our successful clinical trial of suramin in autism, we found that we could correct all the symptoms of autism in mouse models. There are no mousemodels of ME/CFS.
    d. 4th: Since the problems that Dr. Davis’s device finds are the result of abnormalities in the plasma that cause the cells to perform abnormally, it
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    is quite possible that suramin given to an actual person might work on the cells in the body that make the plasma, in addition to correcting the communicationfailures between all the other different types of cells that cause the symptoms of ME/CFS. Once the cell signaling (communication) problems are fixed bysuramin, and eventually by drugs that work like suramin, then the symptoms of ME/CFS might improve. Only a clinical trial will be able to test this.
    e. 5th: Our work is not about suramin per se. It is about the principle of using “antipurinergic therapy” (APT) to help cells heal. Suramin is just the first drugof its kind that works by inhibiting the loss of ATP through channels in the cell membrane, and helps signal through receptors that the final stage of healing canstart. Eventually, there will be a shelf-full of antipurinergic drugs (APDs) that work like suramin. But for now, we only have one.
    2. How will you screen patients for the trial? Which diagnostic/screening criteria will you use? There is a lot of concern about mixing apples and oranges in clinical trials involving ME/CFS. How will you work to address some of the problems that have arisen from past studies that were undermined by patient heterogeneity?
    a. The first study will be in 10 females with ME/CFS who meet the National Institute of Medicine (IOM) criteria for diagnosis. The IOM reviewed andincorporated many elements from the CFS-International Consensus Criteria (ICC), Canadian, and Fukuda/CDC criteria for diagnosis. We plan to enroll patientsthat have symptoms in the middle 80% of all patients with ME/CFS—not the mildest 10%, and not the most severe 10%.
    b. We have learned from metabolomics that although there are dozens of different stresses that can trigger ME/CFS, these are all just different paths to thesame disease. People with the same “core symptoms” of ME/CFS have the same metabolic abnormalities. It doesn’t matter whether the trigger was EBV,HHV6/7, Lyme, Enterovirus, organic solvents, a pesticide, or an industrial metal or solvent exposure. Once you develop ME/CFS, the same core symptomsare present.
    c. A major misconception in medicine is that diseases that are “caused by different triggers are different diseases”. I believe this is wrong. The vast majorityof chronic diseases are caused by the body’s response to
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    stress or injury, and not the initial injury itself. In other words, over half of all chronic disease is caused by blocks in the healing process caused bypathological persistence of the cell danger response (CDR). This is a categorically different way of thinking. It is different from the way doctors are trained tothink about treating “acute” diseases like a strep infection, a broken leg, or a heart attack. “Chronic” disease needs to be analyzed and treated in a completelydifferent way.
    3. How many patients?
    a. The first suramin CFS1 study will be a pilot study of 10 females.
    4. How might the subsets concept in ME/CFS influence the outcome of your clinical trial? How will you address the possibilities of different subsets being includedin the initial study (as per question #2)?
    a. Our hypothesis is that the root cause of the symptoms of ME/CFS is a treatable metabolic syndrome that keeps people in a dauer-like state. I believe that tosubdivide people on the basis of what triggered their CFS years ago, or on the basis of whether they have a common polymorphism in a gene like MTHFR, orwhether they have fibromyalgia, or brain inflammation or not, leads to false classifications. While there are certainly subsets or subpopulations that we candivide ME/CFS patients into based on symptoms, genes, or triggers, these subsets are not based on differences in the root cause of the disease. The signs andsymptoms of CFS are more like slightly different fruit being produced by the same tree. Treating the root problem helps to normalize all the symptoms, regardless of the particular trigger that led to the disease.
    b. The most important medical decision is to determine if the person has an active infection or not. If yes, this must be treated. If there is not an active infection, then we also need to determine if they have a household or occupational exposure to toxins that is ongoing. If the answer to both investigations is “no”, then thepatients would be eligible for the first pilot study. Since our hypothesis is that antipurinergic therapy with suramin will treat the root problem of ME/CFS thatis common to all patients, then you could say that the hypothesis we are testing in the first small pilot study of 10 patients, is that purinergic signalingabnormalities are common to ALL patients with ME/CFS, regardless of any “subset” they might belong to.
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    5. Details about the timeline for a clinical trial with Suramin: when funding is in place, when can it start, how long will trial take, how long to publish, and what willbe next steps if the trial is a success?
    a. People tend to underestimate the cost and complexity of conducting rigorous clinical trials. In the case of suramin, we have learned that to avoid disruptionsin the availability of drug from Bayer, we will need to partner with a commercial sponsor who wants to develop suramin for the treatment of ME/CFS and iswilling to fund the clinical trials. The cost of Phase I/II clinical trials is anywhere from $40,000 per patient to $120,000 per patient. In the case of our firstautism clinical trial of suramin—the SAT1 study of 10 children—it cost $1.2 million. When we were unable to raise money for the SAT2 study, the team of 30clinical investigators that we assembled had to go back to their other jobs, and we lost momentum, as well as cost-savings that would have been possible if wecould have kept the team together.
    b. Because ME/CFS is simpler to study than autism, I estimate the CFS1 study of N = 10 patients will cost about $400,000. When I say “simpler” than autism, I am referring to the technical complexity in selecting outcome measurements. In CFS, the meaningful outcomes are to increase the physical capacity foractivity without malaise, improve sleep, and to decrease the episodes of brain fog and pain. The new commercial sponsor for the ME/CFS studies will need tobe the same company that wants to develop suramin for autism. The first committed step for the new commercial sponsor is that they will need to make their own suramin. This might take another 2 years.
    c. The CFS1 study of suramin will look at 2 doses of suramin over 2 months, with a final blood draw and examination after 4 months. The typical time afterthe completion of the trial to full data analysis, writing the paper, and publication, is about 1 year. Once the funding is available, it takes about 6 months to getall the regulatory approvals and to assemble and coordinate the clinical investigation team. It then takes about 2 months to recruit, screen, and enroll 10subjects in the CFS1 trial. The last patient enrolled, will complete the 4-month study about 6 months after the first patient was enrolled. So from theavailability of funding to publication of the results for the 6 month CFS1 study will take up to 2 years.
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    i. It is important to note that it is unlikely that 2 doses of suramin in 2 months will “cure” ME/CFS permanently. A cure of a disease that has beenpresent for years to decades will likely take a few more doses of drug. All of the significant benefits of drugs like Rituximab took more than 6 months oftreatment to see durable benefits. We expect that 2 doses of suramin in 2 months will produce significant improvements in all the core symptoms ofME/CFS, but that these will wear off as the drug wears off over another 2 months.
    d. If the CFS1 trial is successful, then several more and larger clinical trials will be needed. Many additional questions are answered in these developmentalPhase II trials. Do men and women respond equally well? Does suramin interact with any drugs that are commonly taken by patients with ME/CFS? Theseadditional Phase II studies can take another 3 years after a successful CFS1 Phase I/II study. If no safety issues are encountered and suramin is found to beeffective when given as a few doses over about 6-month, then a pivotal, multi-center, Phase III trial could be started in about 4 years. The Phase III trial mightinvolve 10 different medical centers and perhaps 200-300 patients, take 2 years from start to publication, and cost $10-$20 million. Since the Phase II trialsleading up to this will cost about $10 million, the total cost of suramin drug development, from Phase I/II to Phase III trial is $20-$30 million.
    e. The current market price for an adult dose of suramin is about $54 for a year’s supply (about 10 grams), so the cost of the clinical trials has nothing to dowith the cost of the drug. Typically, it takes 15-30 people on the clinical investigation team at each medical center to conduct a Phase III study. The main costof the clinical trial is the salaries of the staff.
    Questions about the mechanism for Suramin:
    1. There were a lot of questions about the cell danger response (CDR). Some people questioned whether it is wise to attempt to switch off the CDR if it is protective. A faction of group members was concerned that if the protective effects of CDR are removed, and has fear over what might happen in a patient with a re-activated viral infection? There is an idea floating around that
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    Suramin could actually harm people in this situation. What if it’s not just a case of a hit-and-run virus or type of insult. What if the trigger is ongoing?
    a. People should take a look at our animation of the CDR on youtube: https://www.youtube.com/watch?v=zIdUufy8Lks. Imagine a cell as a water balloon filledwith energy. In ME/CFS, the balloon has thousands of pin holes in it that allow precious ATP (energy) to leak out into tissues. Suramin works in two ways.There is a rapid effect and a long-term effect. The rapid effect of suramin can be seen within hours of the first dose. Suramin “plugs” the holes in the cell so ATPis no longer lost. This instantly makes more ATP available for use inside the cell. The long-term effects of suramin are produced by binding to cell surface purinergic receptors. Binding of suramin to these receptors sends a message to the cell that “the war is over” and gene expression can not be changed for healingand growth and mitochondria can go back to their peacetime functions.
    b. Suramin does not “switch off” the CDR. It just restores the CDR to normal balance so healing can start again. We tested if suramin had any affect on thefrequency or severity of infections in the children with autism in the SAT1 study. Two of the placebo children came down with colds during the winter of thestudy, and two of the suramin children did too. There was no difference in the length or severity in symptoms between the two groups. People often forget that the immune system of patients with ME/CFS is not just down, it is unbalanced and dysregulated. We believe that suramin will restore balance between T-cells,B-cells, and NK cells. When balance is restored, the risk of “reactivation” of latent viruses should be less than during the normal course of untreated ME/CFS.We won’t know the full answer to these question until we conduct the clinical trials, but at the low-doses of suramin that we will use to treat ME/CFS, I think thisrisk is low.
    c. As mentioned above, the first question that needs to be asked with any patient with ME/CFS is, “Is there an ongoing infection?” We have many state-of-the-art tools like PCR that allow this question to be answered with very high confidence. Many more medical mistakes occur because doctors “assume facts not inevidence” than by acting on actual facts from rigorous tests.
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    2. In general, a little tutorial about what the cell danger response is would be helpful. Do you have an analogy that a lay person could understand? Then use theanalogy to talk about how Suramin might fix the problem? A clear scientific explanation and a good lay explanation will go a long way toward clearing up many ofthe questions received.
    a. On the one hand, the CDR is nothing more than what we all observe our bodies do when we get sick. When the sickness involves the whole body, as in a caseof the flu, our bodies ache, we have headaches, are more sensitive to light, sound, touch, don’t want to eat much, and don’t feel like interacting socially, or eventalking very much. Sometimes we become obsessive and cranky. Our sleep is fragmented and non-restorative, and the littlest exertion wipes us out. This iscalled “stereotyped sickness behavior”. It is not caused by a particular virus or a particular virus or mold infection. But it can be triggered by any of them.These symptoms are caused by a generic response that our cells have to systemic infections of many different types. This stereotyped sickness response isactually produced by characteristic changes in the chemistry of the body that make up our metabolism. We have studied these changes on a machine called amass spectrometer.
    i. We found that all 8 of the complex diseases that we have studied in the past 3 years (autism in 2 different studies, PTSD, TBI, Gulf War Illness, MajorDepressive Disorder, Primary Sclerosing Cholangitis, and ME/CFS) had abnormalities in the same shared core pathways. These are the metabolicpathways of the different stages of the CDR.
    b. My lab discovered the metabolic features of the CDR and gave it the name, “cell danger response” in 2014. I recommend reading our paper that you candownload from our website at: http://naviauxlab.ucsd.edu/publications/. I will be publishing more over the next year about how the CDR is used to start thehealing process after any injury or infection. The start of the CDR is normal and necessary. Chronic disease results when the body is unable to reset the CDRafter the danger has passed.
    3. Can you share with us what you think the side effects of Suramin might be for an ME/CFS patient (based on the autism study and African sleeping sickness patients)?
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    a. The dose we will use in ME/CFS is 1/5th the dose that has been used for African sleeping sickness for 100 years, and 1/25th the dose that was used to treatcertain resistant cancers in the 1990s and early 2000s. Most drugs have side-effects at high doses that are not seen at low doses. Imagine for example, if adoctor told you to take 50 aspirin for a headache. 50 tablets of aspirin can send you into a coma, but 2 aspirin are safe and effective for treating a headache. Noone has ever studied suramin at the low doses that we will be using, so I can’t say what the side effects might be, if any. When used at the high-doses needed tokill cancer cells, about 10% of people developed side effects each month until by 5 months, about 50% of people had one or more symptoms like a peripheralneuropathy (tingling in the hands or feet), adrenal insufficiency, or anemia. We didn’t see any of these symptoms when we used low doses of suramin inchildren with autism.
    4. Are there other treatments that might or might not affect CDR? Do other treatments for ME/CFS affect CDR to your knowledge?
    a. Eventually, we will have a shelf-full of antipurinergic drugs (APDs) that work like suramin, but have slightly different properties that doctors can pick fromto match to the needs of each patient. Some APDs are being studied in clinical trials of rheumatoid arthritis, but none of them is available yet for medical use.Like the first antibiotic, suramin is just the first drug of its kind.
    5. Do you have reason to suspect that gains from Suramin will be lasting? So many treatments seem to be beneficial initially but the gains are often lost. Do youthink Suramin will be different and, if so, why? (one member cited Jay Goldstein’s work on CNS and peripheral nervous system).
    a. I believe that after a few months of treatment, the healing process can get started again and ME/CFS patients might improve enough to get back to morenormal lives. In the beginning, once the first energy is restored, then a program of good food and activity will be possible. Just as a broken leg that has been ina cast for 6 weeks is a little deconditioned, so will the patients with ME/CFS. But soon, the gains will become self-sustaining, and chronic suramin will not berequired. Each person with ME/CFS has certain genetic and metabolic characteristics that will make them more vulnerable to relapses than someone who hasnever had ME/CFS. However, I believe that with care, physiologic reserves can be
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    strengthened, and many potential triggers that might cause a relapse can be avoided. But if a relapse occurs, a short course of an APD might be all that isnecessary to abort a full relapse. We won’t know if any of this is possible until we do the science and conduct the clinical trials.
    Questions about drug availability:
    1. Are you working with other drug companies, even Canadian ones, to produce Suramin (now that patent has expired?). If the trial is successful, presumably therewill be increased demand. How is this being addressed?
    a. We are in negotiations with a commercial sponsor who is planning to make all the suramin we need for the clinical trials. Because of the high cost ofclinical trials, the same company that makes the suramin and the one that pays for the trials need to be the same. We have encountered interruptions in bothfunding and drug supply when these two are disconnected.
    2. What role might Bayer play in this study? None.
    Questions about how much funding is needed and how that funding would be used:
    1. What kind of funding do you need? Can you give us a break down, prioritizing items? (money for clinical trial, money to hire staff, money for lab maintenance, etc…how much does it cost to do a study like this, inclusive of other costs (i.e. indirect costs) to the lab? In other words, what is the cost of doing business in theNaviaux Lab?
    a. The basic cost for salaries and equipment in my lab of myself and 3 scientists and 2 mass specs is $800,000 per year—about $70,000 per month. I have tobring in all of this from gifts and grants. My university does not provide this. Not even the salaries are paid by UCSD.
    b. Any clinical trial is an added cost. As I mentioned above, the first Phase I/II autism study of suramin cost $1.2 million. The first Phase I/II of suramin inME/CFS will cost about $400,000. If successful, it will take another 3-4 trials culminating in a multi-center Phase III trial of suramin in about 10 centers and200-300 patients with ME/CFS. The total cost of clinical trials over the next 5 years would be about $20-30 million.
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    c. The high cost of clinical trials for drug development is why virtually all drug trials are sponsored by Big Pharma, or biotech startups. Even NIH does nothave the resources for supporting large clinical trials.
    d. I will be applying for the FDA “rare disease drug development” program to develop suramin as a possible treatment for primary mitochondrial disease(PMD). This is a special program from the FDA Office of Orphan Products Development (OOPD). However, since CFS and autism are not rare diseases, theydo not qualify for this program.
    2. What is the relationship between OMF and your funding? How do researchers qualify for funding from OMF? Does hearing from patients at OMF or SolveME/CFS help shape funding priorities? If not, how could it?
    a. The OMF provided 1 year of funding to support a metabolomics validation study of ME/CFS. The funding for that study is now over, but we will continueworking on it free of charge until we can submit a manuscript for publication by the end of this year.
    b. We do not have any current funding from the OMF.
    3. What other funding sources are you exploring? What else is out there? What is needed, in your opinion, to access these funds? Pilot data?
    a. I think the only plausible funding sources for the magnitude of funding needed for clinical trial development are commercial sponsors, Big Pharma, or asingle philanthropist with significant capacity.
    4. We are discussing a croud-funding campaign strategy. What do you think would be most effective in a campaign like this? Would you be willing to make a videoor provide some quotes to help with a crowd-sourced campaign?
    a. Crowd-funding works for tens to hundreds of thousands of dollars— typically less than $0.5 million. It is unsuccessful in raising millions or tens ofmillions needed for clinical trials.
    5. These sorts of crowdsourcing campaigns are more successful when there are itemized funding milestones. Can you break down the components of a clinical trialand attach a price tag to them?
    a. The first milestone would be $800,000 for 1 year of funding for the lab. b. The 2nd milestone would be $400,000 for support for the CFS1 pilot
    study.
    c. Currently, I spend 90% of my time looking for money for the lab. This is time that I cannot spend on the actual science. A philanthropic commitment for $1million per year for the next 5 years would allow me
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    to refocus on the science and would dramatically accelerate the pace of discovery.
    6. Assuming the trial is successful and results point to a phase 3 trial, what kind of money are we talking about for that? How do you go from a small clinical trial to aphase 3 trial?
    a. $10-$20 million for the Phase III. See above
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  4. CFS_for_19_years

    CFS_for_19_years Hoarder of biscuits

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    I wasn't able to log in using my Facebook credentials, and since that page looks iffy, I've changed my Facebook password. I'll try after the link is fixed or whatever.
     
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  5. RL_sparky

    RL_sparky Senior Member

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    The link works for me but others were having problems so I just copied and pasted.
     
  6. RL_sparky

    RL_sparky Senior Member

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    I'll see if I can get that info tomorrow.
     
  7. Neunistiva

    Neunistiva Senior Member

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    Isn't this the answer?

    "5. These sorts of crowdsourcing campaigns are more successful when there are itemized funding milestones. Can you break down the components of a clinical trial and attach a price tag to them?

    The first milestone would be $800,000 for 1 year of funding for the lab. b. The 2nd milestone would be $400,000 for support for the CFS1 pilot"
     
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  8. Jesse2233

    Jesse2233 Senior Member

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    Good catch

    But perhaps something more achievable short term could act as a bridge to getting more funds
     
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  9. CFS_for_19_years

    CFS_for_19_years Hoarder of biscuits

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  10. melihtas

    melihtas Senior Member

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    Yes, it is identical as long as it is called Suramin Sodium Salt and has this structure.

    [​IMG]

    There are also slightly modified versions of the molecule (its analogs) and there are some in vitro studies saying that those analogs are more effective in lower doses with less side effects but they have never been tried in humans, so, we should stick to the original molecule.

    Keep in mind that administering Suramin from chemical suppliers is not as easy as Suramin by Bayer. Bayer's Suramin (Germanin) comes as powder in 5 ml vials to easily make the solution but chemical suppliers send it in a plastic bottle. Suramin quickly deteriorates when it contacts with air. You can only open those bottles in nitrogen atmosphere to prepare the injectable solution.
     
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  11. Murph

    Murph :)

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    Thanks a lot @RL_sparky . The funding side of things is depressing really. As Naviaux notes, the amounts needed are really more than the patient community can easily provide.

    We need government and business to fund it, really. Time spent fundraising may not be as worthwhile as time spent advocating.
     
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  12. Jesse2233

    Jesse2233 Senior Member

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    I wonder about direct appeals to Bayer and Walter Koroshetz. Maybe a petition would be a good place to start
     
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  13. Jesse2233

    Jesse2233 Senior Member

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    So you would need to administer it using a lab? What comes next after one opens the bottle?
     
  14. melihtas

    melihtas Senior Member

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    You don't need a full scale lab but at least you need something like this. A DIY version of this can be made at home if you know what you are doing.
    [​IMG]

    Once you open the bottle, you mix 1 gr Suramin with 10 ml water and shake it vigorously to dissolve it. Now, you can inject it intravenously. Since it is cytotoxic (toxic for cells) at high concentrations, you should inject it slowly over 15 minutes allowing it to spread into the blood.
     
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  15. Skycloud

    Skycloud Senior Member

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    I hope you don't mind @RL_sparky, but I've reformatted your post to make it easier to read. No other changes.

     
  16. RL_sparky

    RL_sparky Senior Member

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    Yes, the funding issue is depressing and the amounts needed are more then the community can generate. I know it takes about $70,000 a month just to keep Naviaux's lab doors open. He has some other funding so I don't know what kinda monthly shortfall he has. I will try and find out.
    We really need to organize better as a community and put pressure on our governments as they have the ability to provide funding opportunities. Were at a point where there are promising research leads with a lack of money the main obstacle to figuring this disease out.

    @Skycloud Thanks for editing it!
     
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  17. Skycloud

    Skycloud Senior Member

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    You're so right.
    Naviaux, and other searchers should not be using their time in this way. It's depressing to read this. I would like to see more of our collective energy on PR used for advocacy and fundraising but I know it's easier said than done. I don't want to downplay what has been achieved by so many already, often at cost of their health but I do feel frustrated, not least with myself.
     
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  18. RL_sparky

    RL_sparky Senior Member

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    Regarding CrowdFunding, Dr. Naviaux has this to say: Thank you for your support. Anyone can “crowd so...urce” their support for our lab at: http://naviauxlab.ucsd.edu/support/
    All they need to do is pull out their credit card and make a donation to any of three different projects.
    There are strict rules about using commercial crowd-sourcing software at the university. These rules are only recently being expanded to permit some types of software, but not others. It turns out to be more of a regulated space than you might imagine; easy for non-academics, but harder for professors working at the university.
     
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  19. Jenny TipsforME

    Jenny TipsforME Senior Member

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    You're right this is depressing, not a good use of his skills at all :(

    Philanthropy sounds :angel: though hard to make the right connections. It would probably require less paperwork for monitoring too, which would also save his time. Anyone know anyone both very rich and very generous?! Or any Philanthropy Advisors?
     
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  20. perrier

    perrier Senior Member

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    Yes petition a great idea
     

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