Galectin Therapeutics- sifting through the ashes, to figure out what started the fire

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Galectin Therapeutics Scientific Investment Thesis

Sifting through the ashes, to figure out what started the fire

by

Team Scientific

Disclaimer:

Investment returns may go up as well as down according to market conditions beyond our control. Our views are not an invitation to treat, nor are they meant to be relied on. Every due diligence we develop is a document that we use for my own investment purposes. Please use this blog to supplement your own investment decisions, at your own risk, and according to your own criteria.


Investment Strategy:

Investing in biotech/pharma companies is a high risk, high reward venture that puts most common investors at an increased risk when compared to their professional counterpart. Price fluctuation for small-cap stocks is heavily facilitated by short-term market sentiment over trivial factors, which at times can be counter-intuitive.

It is imperative to understand that almost all biotech companies are developed from a pure speculative standpoint: they have no product, very limited data, but they need money to continue to conduct research, thus they will pull every possible method to obtain funding. Some companies will bring on famous biotech leaders to their scientific advisory board to attract investors, gain market attention, and to network their way toward establishing a fund large enough to conduct experimental or clinical studies. Unlike the tech industry, where the product directs a company’s success, the biotech industry will proclaim that an idea has potential for company success. However, investing in an idea is very high risk.

We believe that a strong strategy is to invest with a long-term mindset to help mitigate the short-term risks.  Strong science and strong business practices are two quantitative factors that provide a proper analysis regarding company growth and direction. The former requires specific expertise within the scientific field, and because the general public is more in tune with the company’s business practice, the company will oversell their science to gain market and investor attention.

We will primarily analyze the scientific or clinical data that drives every company, and present to you a dissertation that you can use to help facilitate your decision to invest. Unless otherwise stated, we will not present any news or technical analysis, such as daily chart observations, trend-lines, channel analysis, etc. because these factors are fueled by short-term interests, and ultimately subject to personal and emotional bias.


Background:

The fundamental science that embodies Galectin Therapeutics is driven by Glycobiology. Glycobiology is the field of carbohydrate (glycan) chemistry and biochemistry. In brief, carbohydrates are defined as complex molecules (polysaccharide) that are linked together by a number of individual smaller molecules (monosaccharide). The biological roles of carbohydrates are particularly important – from the assembly of complex multicellular organs and organisms, to the interactions between cells and their surrounding matrix, the field of glycobiology is incredibly diverse and essential to all mammalian life.

When we think of a cell, we imagine what we see in textbooks: a circular structure with a smooth outer membrane. This depiction couldn’t be further from the truth. A cell is in fact “hairy”. Many projections (carbohydrates) protrude from within, and into, the cell. These projections are like trees of a rain-forest (glycocalyx), they are incredibly diverse in both structure and function. Each flower, leaf, stem, branch, and trunk of a tree contribute to various cellular roles, and more importantly these projections are what allows our cells to communicate with one another.

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About the Company:

Galectin Therapeutics is a clinical stage biopharmaceutical company that is engaged in the development of carbohydrate-based therapeutics, indicated for  treatment against fibrotic diseases, skin diseases, and cancer.

Unlike the incredible success of small-molecule drug discovery, the discovery of pure carbohydrate-based therapeutics has been incredibly under-studied, despite the establishment that carbohydrates (glycans) have played an important part in the essential structure and activity of many small-molecule therapeutics –  like the antibiotic Streptomycin or the anticancer agent Doxorubicin.

Galectin Therapeutics has two proprietary chemical entities in  current development- GM-CT-01 (galactomannan), and GR-MD-02 (galactoarabino-rhamnogalaturonan), which are novel complex carbohydrate galectin inhibitors indicated for treatment against nonalcoholic steatohepatitis (NASH), cirrhosis, psoriasis, and cancer. 

The following pipeline is listed below:

table2galt
From SEC Form 10K

Perspective

A gamble or an investment?


Scientific Analysis

Cells release and respond to molecules as a means of communicating with one another. One specific molecule, Galectin, is a widely expressed family-class of lectins that bind cellular projections (carbohydrates) at very particular recognition domains (like birds that choose a specific branch to perch on a tree). Upon recognition, galectin binding initiates a wide range of cellular roles that include the development and regulation of immune cell activities, and the microbial recognition as part of the innate immune system. Recent advances have demonstrated that Galectin-3 (a particular type of galectin) is implicated in the pathogenesis of many disorders including, but not limited to, fibrosis, steatohepatitis, cancer, inflammation, and adipogenesis.

The rationalization for use of complex carbohydrate-based galectin-3 inhibitors is backed by evidence for  treatment of the following indicated disease state: fibrosis and nonalcoholic steatohepatitis (NASH).

The table below highlights the conclusive findings per publication.

A. Experimental Studies

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If you take a close look, there is one pressing question that has yet to be answered:

Is inhibition of Galectin-3 truly the mechanism by which GR-MD-02 exerts its therapeutic effects?

It has been clearly stated thatalthough improvement…in the activity of NASH and reduction in fibrosis was associated with reduction in the expression of Galectin-3 protein…it was not necessary to have a marked reduction [of Galectin-3] to observe the therapeutic effect”.

Inhibition of galectin-3 expression is independent from the benefit observed with GR-MD-02 or GM-CT-01-induced NASH improvement in vivo. Furthermore, it has been stated that though “Gal-3 mRNA expression tended to be down-regulated in the treatment groups compared with the vehicle group… levels did not reach statistical significance

In other words, just because galectin-3 is overexpressed in inflammatory or immune disorders, does not indicate that inhibition of galectin-3 will afford any clinical benefit.

Carbohydrate-based therapeutics is incredibly complex, as limitations such as lack of specificity, molecular stability and clinical relevancy hinders drug discovery and development. One common obstacle within the field of Glycobiology any medically-related scientific discipline, is identifying key molecular pathways that directly contribute to a distinct clinical phenotype.

B. Clinical Studies

Clinical trials for each experimental drug is listed below (from SEC FORM 10K). It is clear that GR-MD-02 is the lead drug candidate.

Though the company has presented a very admirable drug portfolio, each of which are in various phases of clinical trials, one should not ignore the fact that (1) The mechanism of action in vivo remains unclear and (2) GR-MD-02 has failed to meet statistically significant primary endpoints in both NASH-FX and NASH-CX trials. 

galtpipeline.png


A closer look at fibrosis…

1. The NASH-FX trial, a Phase 2a pilot trial NASH-FX for patients with NASH advanced fibrosis that explored use of three non- invasive imaging technologies.

The trial did not meet its primary biomarker endpoint as measured using multi-parametric magnetic resonance imaging (LiverMultiScan(R), Perspectum Diagnostics). The trial also did not meet secondary endpoints that measure liver stiffness as a surrogate for fibrosis using, magnetic resonance-elastography and FibroScan® score.

2. The NASH-CX trial, a larger well-designed multi-centered clinical study that assessed the therapeutic efficacy of GR-MD-02 against liver fibrosis and portal hypertension in patients with well-compensated NASH cirrhosis, did not meet their primary endpoint with statistical significance  in 162 patients across 36 sites in the United States.

They did, however, find statistical significance in a post-hoc analysis (after failing to reach statistical significance, additional analysis were performed to find a significant correlation between therapy and clinical outcome)

Key NASH-CX findings are reported below (SEC Form 10Q):

“(1) GR-MD-02 had a statistically significant and clinically meaningful effect in improving hepatic venous pressure gradient (HVPG) vs placebo in patients with NASH cirrhosis who did not have esophageal varices at baseline; this effect was seen regardless of the patient’s baseline portal hypertension. Furthermore, we believe that patients with esophageal varices may have masked benefits in the total patient population

Picture1
The GR-MD-02 2 mg/kg group showed a statistically significant reduction in HVPG from baseline to week 54 for patients without varices– Final NASH-CX Data Presentation 2017

Question to consider: what does improvement of HVPG have anything to do with providing a clinical meaningful effect in NASH patients?

The FDA questioned the clinical meaningful effect of HVPG changes and did not grant the company “breakthrough designation” for GR-MD-02, due to the fact that further confirmatory data is needed to identify the level of change in HVPG that is reasonable likely to predict clinical outcomes”

(2) There was an important drug effect of GR-MD-02 in the total patient population on liver biopsy with a statistically significant improvement in hepatocyte ballooning (ie cell death)

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There was a statistically significant improvement in ballooning in both treatment groups compared to placebo – Final NASH-CX Data Presentation 2017

Question to consider: If investigators can stratify their population data to patients without esophageal varices (1), what would the data look if hepatocyte ballooning was also stratified to the same subset of the total patient population? Significant? Insignificant?

(3) There was a statistically significant reduction (p = 0.02) in the development of new esophageal varices in drug-treated patients compared to placebo; we believe that this is a clinically relevant endpoint related to patient outcomes

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Significantly fewer new varices developed in treatment group –Galectin Corporate presentation 2018

Questions to consider: Was this an initial clinical endpoint? Or did investigators present this data after failing (1)?

If indeed this is the case, presenting data that was not initially implicated as a clinical endpoint may serve as a strategic ploy to counter insignificant data with a “beside-the-point” statistically significant analysis.

Take a look at the Final NASH-CX Trial presentation and note the following slide:

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Final NASH-CX Data Presentation 2017

It is not scientifically sound to play around with data to fit ones hypothesis. If GR8 did not show any therapeutic efficacy with regards to NASH, then GR8 should not be used as a means to increase statistical significance when assessing the development of esophageal varices. Why not compare GR2 to placebo?

(4) There was a drug effect in both the 2 mg/kg and 8 mg/kg dosage groups on liver biopsy and in the mild portal hypertension group, there was a consistently greater and statistically significant effect of the 2 mg/kg dose of GR-MD-02.

Question to consider: If the proposed mechanism of therapeutic efficacy is Galectin-3 dependent, why is there not a dose-dependent relationship?

(5) The apparent lack of a dose response in the GR8 group may be explained by variable pharmacokinetics in the high dose group, and this suggests use of an additional and intermediate dose between 2 and 8 mg/Kg in subsequent trials.

Question to consider: Is it possible that the lack of dose response suggests that the therapeutic efficacy is not dependent on Galectin-3 inhibition (as observed in the experimental publication?) Benefit observed may be an off-target effect = esophageal varices?

(6) GR-MD-02 appears to be safe and well tolerated in this one year clinical trial

(7) Investigators believe this is the first large, randomized clinical trial of any drug to demonstrate a clinically meaningful improvement in portal hypertension or liver biopsy in patients with compensated NASH cirrhosis without esophageal varices.”

NASH Conclusions:

Unfortunately, the positive conclusions they are presenting do not support the endpoints that were designed to assess the clinical success/failure of GR-MD-02. The company’s early experimental studies have all failed clinical trials. Any information beside that point should be considered as a strategic move to urge  investors to focus primarily on forward-looking statements, as opposed to the concrete evidence that has been clearly under-represented.


A closer look at plaque psoriasis…

The  plaque psoriasis trial began after making an observation in the NASH-FX trial in a single patient. “During our Phase 1 NASH fibrosis trial with GR-MD-02, a clinical effect on plaque psoriasis was observed in a NASH patient who also had this disease. This patient had marked improvement in her psoriasis, with improvement beginning after the third infusion. She reported that her psoriasis was “completely gone” and her skin was “normal” after the fourth infusion. Her skin remained normal for 17 months after the final infusion of study drug. The patient is convinced that the improvement in her psoriasis is related to the study drug.”

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All 5 patients treated in phase 2a open label trial showed improvement in disease activity by an average of 50% (one improved by 82%) – Galectin Corporate Presentation July 2018

Plaque Psoriasis conclusions:

Despite the interesting results, “there are already existing drugs on the market in this disease that produce greater efficacy and higher improvements in 60-90% of the patient population”. 


A closer look at cancer immunotherapy…

Immuno-oncology is a vastly growing field within the cancer field. In brief, immune cells are harvested from the cancer patient and re-administered as a method of boosting the patients immune system against their own cancer cells. One particular challenge regarding immunotherapy, however, is the reduced efficacy, in part, due to the tumor micro-environment- a complex ecosystem involving multiple immuno-suppressing factors.  It is thought that the galectin-3 plays a major contributing role.

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Rabinovich G, Nat Rev Immunol, 2009

To date, both cancer clinical trials are currently under clinical investigation. 

1.Phase IB Study of a Galectin Inhibitor (GR-MD-02) and Ipilimumab in Patients With Metastatic Melanoma

Goal of study:To determine a safe dose of GR-MD-02 used in combination with the FDA-approved dose of ipilimumab (3 mg/kg) in patients who have advanced melanoma. GR-MD-02 is a galectin. Galectins are a family of proteins that have numerous functions in normal mammalian biology including the facilitation of cell-cell interactions, regulation of cell-death and regulation of immune system responses. The hypothesis is that a safe dose of GR-MD-02 when given with the FDA-approved dose of ipilimumab can be found.

  • Primary Outcome: Determine a safe dose of GR-MD-02 used in combination with the approved dose of ipilimumab (3 mg/kg) 
  • Secondary Outcome: Response rate to combined therapy

Study started in March 2014 with an estimated primary study completion date of December 2018. 

2. GR-MD-02 Plus Pembrolizumab in Melanoma, Non-small Cell Lung Cancer, and Squamous Cell Head and Neck Cancer Patients

Goal of study: “This study will employ a 3+3 phase I design with dose escalation of GR-MD-02 in conjunction with the standard therapeutic dose of pembrolizumab in patients with advanced melanoma who have had progression after ipilimumab and/or BRAF targeted therapy when a BRAF mutation is present, non-small cell lung cancer patients with disease progression after targeted therapy, or head and neck squamous cell carcinoma patients with disease progression after at least one platinum-containing regimen. In addition to monitoring for toxicity and clinical response, blood and tumor samples will be obtained to assess immunologic measures relevant to galectin biology and pembrolizumab T-cell checkpoint inhibition.

  • Primary OutcomeFrequency and severity of treatment-related adverse events measured by common terminology criteria for adverse events
  • Secondary Outcomes: 1- Measure the response rate to combined therapy with GR-MD-02 and pembrolizumab in patients. 2- Assess the biological activity of GR-MD-02 in combination with pembrolizumab.

Preliminary results were released in September of 2018: Investigators are utilizing the Response Evaluation Criteria in Solid Tumors.

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N=13; 1 patient in cohort 3 not depicted due to clinical progression prior to scans. Dotted line at -30% change from baseline indicates the RECIST 1.1 threshold for definition of partial response

The mechanism of action of their lead candidate GRMD02 is not only unknown, but demonstrated no significant efficacy in their primary disease indication = NASH. Though failure in NASH does not mean potential failure in the cancer trial, it does however provide more questions regarding company focus than answers. What makes the investigators confident that GR-MD-02 will inhibit Galectin-3 in patients suffering from cancer? Unfortunately, the cancer immunotherapy trial more of a gamble, as opposed to an investment. 


Investment Due Diligence Conclusion:

Multiple ongoing shareholder derivative action lawsuits, lack of funding past the first quarter of 2019, and lack of company foresight, puts investors at an incredibly high risk compared to other competitors in the same field.

Is this investment scientifically or clinically sound?

We applaud the investigators for the amazing work and effort they put into developing a drug that addresses an unmet clinical need. However, the ambiguity regarding GR-MD-02’s mechanism of action in vivo is a major red flag in NASH experimental models. In addition, galectin-3 levels did not correlate with therapeutic efficacy, and a lack of dose response suggests an alternative mechanism of action that may be gal-3 independent. Such limitations may have contributed to  failure of P2 NASH clinical trials. Furthermore, we found that investigators stratified certain patient populations in their post-hoc clinical data analysis in such a way that increases statistical significance. Currently, this company does not qualify as a viable long-term asset. It does however, make for a great high-risk/high-reward gamble via anticipation of immunotherapy clinical data and/or announcement of NASH P3 partnership.


 

14 thoughts on “Galectin Therapeutics- sifting through the ashes, to figure out what started the fire

  1. You guys really want to learn about science and how gal3 promotes the development of various deseases refer to link below. 9 Phd’s with years of research. Oh and btw Galt has the drug which inhibits gal3. Your welcome.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855601/

    1. Hi Gabriel,

      Thank you for the comment. We don’t refute the potential role for galectin-3 to contribute to the pathogenesis of NASH or tumorigenesis. Our concerns only revolve around the stated fact that (1) “inhibition of galectin-3 is not required to observe a therapeutic effect” and (2) “Gal-3 mRNA expression tended to be down-regulated in the [GR-MD-02] treatment groups compared with the vehicle group, although the levels did not reach statistical significance”

      The above statements can be found in the company’s experimental publication: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3867460/

      Best,

      JWS, PhD

  2. Thank you! short thesis is solid. One of the main questions is whether the company will get bought out. I’m guessing this thesis wasn’t too difficult to tease out. What are the chances of a buyout? Chances of further dilution or…chances of chapter 11 when they run out of money at the end of May?

    Thank you.

    1. Hi Andrew,

      Thank you very much for your questions. Our expertise only encompasses the quality and integrity of the science at hand, and the likelihood of clinical success given the data presented. Given this, we are not able to provide any reliable or confident statements regarding the chances of a buy-out, merge & acquisition, dilution, or filing of chapter 11. In our honest opinion, the above questions will most likely be answered as more cancer data is presented by the company. That said, the company needs to obtain capital by May 2019, thus they need to pull any possible method to do so. The easiest yet most unfortunate way, is dilution (this of course our opinion and completely speculative). However, here are certain points that may help indirectly answer your questions:

      1. A trial with Keytruda (Merck) presents a speculative possibility of potential partnership, but unfortunately significant positive data is required. As noted in our post, positive data has historically been lacking in clinical trials

      2. With respect to the Psoriasis trial, the company is looking to “entail a controlled, does-ranging clinical trial”, which they will not proceed without a strategic partnership (SEC Form 10Q). Psoriasis however, does not seem to be their lead disease indication. Furthermore, there are already drugs with greater efficacy in the market.

      3. With respect to NASH, we find no statements (to our knowledge) made in SEC filings regarding partnership, except that the company is discussing with the FDA for Phase 3 trial logistics.

      I hope you can understand that our focused expertise prevents us from providing you with confident claims that may answer your questions!

      Best of luck,

      JWS, PhD

  3. fpbear

    JWS, your main concern is your statement “The company has not determined the mechanism of action.” You give this as the reason why GALT would be a gamble for both NASH and cancer. About a month after you wrote this article the company has created a lengthy presentation to specifically explain the mechanism of action of GR-MD-02. Your article is much less detailed than the company’s presentation on the mechanism of action. Here is the company’s presentation that should clarify some things you may not have had enough time to research:

    http://galectintherapeutics.com/wp-content/uploads/2018/11/AFDD-slides-GALT-FINAL-29Nov18.pdf

    1. Hi fpbear,

      Thank you for your comment. We are aware of the latest presentation, here was our issue with the presentation:

      1) 75% of the presentation is discussing background information regarding galectin-3

      2) 25% of the presentation split between discussing the mechanism of GR-MD-02 and the clinical results

      3) All of the experimental mechanistic data is from a single paper published many years ago by the company’s former CEO

      4) Cherry picking of the data in the presentation:

      The company picked certain aspects of the paper to maintain a certain narrative. For example on slide 28, the presenter claims that “Treatment with GR-MD-02 Markedly Reduces Gal-3 Expressing Macrophages in NASH Mice”, and shows data to support this claim. What the presenter is not showing, however, is that the same paper that the data was taken from also states that “…in the late treatment cohort of the same experiment, Gal-3 mRNA expression tended to be down-regulated in the treatment groups compared with the vehicle group, although the levels did not reach statistical significance”.

      This is contradicting data, where an insignificant decrease in mRNA gal3 expression upon GR-MD-02 treatment was observed, as well as a significant decrease in gal-3 antibody staining via immunohistochemistry (IHC). Why did the presenter choose to only show the IHC data and not the mRNA data? It would be more straightforward if the authors stated: “no significant reduction in gal-3 mRNA expression was observed, interestingly we detected a significant reduction in gal-3 antibody staining”. The scientific community would much rather favor the more quantitative data (mRNA expression levels) as the reputable data to interpret. The reason is because the IHC data is rather descriptive, the authors are only showing a single image of a very small snippet of the entire liver, which may not truly represent the levels of gal-3 expression (mRNA detection, however is looking at total liver gal-3 expression)

      5) Nowhere in this presentation does it state that their Phase 2 NASH study failed to meet their own initial endpoints, yet are making claims based on a contrived set of clinical data

      I hope this helps with understanding as to why we chose not to include this presentation in our due diligence = it is the same data that we have already analyzed.

      Best of wishes,

      JWS, PhD

      1. fpbear

        It still doesn’t make sense how your conclusion of “company does not qualify as a viable long-term asset” follows from the very minor lack of understanding that your team has. That seems like an extreme conclusion just because there are always, inevitably, a few unknowns about complex cell biology. The scientific community has now well characterized how Rhamnogalacturonan binds to inhibit Galectin-3, for example see “Novel polysaccharide binding to the N-terminal tail of galectin-3 is likely modulated by proline isomerization” https://academic.oup.com/glycob/article/27/11/1038/4080185 If your conclusion is correct, that would mean not only the immunohistochemistry is a fluke result, but also the plethora of papers describing Rhamnogalacturonan mechanism of Galectin-3 inhibition are also in error.

      2. Hi fpbear,

        Thank you for the comment.

        Please note the blue highlighted statements that refer to why we consider GALT more of a gamble (MOA issues, insignificant clinical findings, poor financial health, psoriasis not a lead candidate, multiple law suits, Grmd02 as the only clinical lead drug, etc).

        We understand that determining the exact MOA is not always a major red flag for each individual person. We do our best to take every opportunity into consideration. For example, we also state that inhibition of galectin-3 may not always result in a decrease in galectin-3 levels. The overwhelming issues is however something that our team can not ignore. It is the job of every company to omit and exclude vital technical or scientific issues that may result in loss of investor interest. It may be illegal to do so financially, but it is not illegal scientifically. Our job is to do our best to take an unbiased approach, and come to a conclusive standing based on the evidence we discover at hand.

        I hope you can understand our approach.

        Best,

        JWS, PhD

  4. fpbear

    GR-MD-02 is one of the very few drugs proceeding to NASH Phase 3 trials so it would be incorrect to say that there are insignificant clinical findings. The pharmaceutical industry has spent many billions to bring their drug candidate into this select group, and this company is one of the very few to succeed to this stage of the race. Phase 1 and 2 results are significant enough that FDA has given the company a path to Phase 3.

    How can this be insignificant? You claim to have an unbiased approach, but I’m sorry to say that I see a LOT of bias!

  5. Hi fpbear,

    We respect everyone’s opinion on the matter and encourage discourse.

    We simply can not state that the company has met phase 1 or 2 clinical endpoints with significance, as the company themselves have clearly stated this in company filings (10K/q). Alternatively, please find the direct links to each clinical trial publication in our post.

    Best,

    JWS, PhD

  6. fpbear

    When you write “compared to other competitors in the same field” — which competitors are you referring to? Since you are completely anonymous and the article contains false scientific assertions that I have pointed out in my comments above, I can only assume that a competitor is funding this hit-piece.

    1. Hi fpbear,

      That statement is made directly by GALT themselves (please find the direct statement made in 10K SEC filings).

      We do not post false scientific assertions, and cite every statement made.

      Lastly, we disclose no financial support from any institution, other than donations provided by our viewers to help us gain better company insight.

      Best,

      JWS, PhD

      1. fpbear

        It is industry practice that stock analysts (and scientific research papers) provide their name, institution, who’s paying for the article, and any financial holdings that would present conflict of interest. You are providing none of this information.

        Yes you do have false scientific assertions, and it is pretty obvious to anyone street-savvy that you have some conflict of interest that is keeping you from being scientifically honest. I brought up these points above but you just sidestep them.

      2. Hi fpbear,

        Please note that we are not stock analysts in the conventional sense. Also, for our free content, our team has currently chosen to remain anonymous to mitigate risk of personal insult as we engage with the financial community. Our hope is to bring scientific due diligence to those who are indeed financially-savvy to help bridge the gap in knowledge. Unlike common review due diligence articles (such as seeking alpha, etc.), we choose to write our work in the form of a thesis. Thus, we are obligated to analyze any life science company from an initial unbiased scientific standpoint, prior to picking what side of the coin we choose to stand on.

        As we develop novel ways to expand our expertise and our platform, we do hope to be able to provide our viewers with credentials and our identity. I hope you can understand that due to the fact that we are scientists who all work full-time within the life sciences industry, putting our opinions and our identity to the common public for free puts our personal and professional livelihood at risk.

        In theory, we can not make scientific assertions given the fact that we are looking at data that has already been peer-reviewed, published, and investigators have already made their claims. If you take a look at our work in greater detail, you will find that we are independently analyzing the published data, and providing our own internal conclusions based on what we find. Depending on our analysis, our work may either agree or disagree with the investigators.

        We hope that for every point you have made, we provide you with direct links to credible sources. Please don’t hesitate to contact us directly via email if you have any additional concerns at: scientificinvestments.usa@gmail.com

        Cheers and happy holidays!

        Best,

        JWS, PhD

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