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Galectin Therapeutics Inc. (GALT)

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  • A
    Mayo Clinic Proceedings, Review of Portal Hypertension 2019

    "Extensive research has identified the molecular and cellular mechanisms involved in the development and progression of liver fibrosis as well as vascular remodeling, the main drivers of portal hypertension. Chronic hepatocellular injury promotes activation of perisinusoidal cells, known as hepatic stellate cells (HSCs), which acquire a fibrogenic myofibroblast phenotype, resulting in collagen production and sinusoidal constric tion. Transdifferentiation from quiescent to activated HSCs is a complex process modulated by various extracellular signals originating from resident liver cells, such as hepatocytes and sinusoidal endothelial cells, as well as inflammatory cells, including macrophages, lymphocytes, and platelets.4 Increased understanding of HSC biology has led to the development of stellate cell targeting drugs, which are currently in phase 2 and 3 human clinical trials, including Cenicriviroc (dual CCR2eCCR5 receptor antagonist),5 GR-MD-02 (galectin- 3 inhibitor),

    Now for the 1000th time.

    Fibrosis under a microscope means little. It's the clinical effects of fibrosis on vascular resistance and portal hypertension that are key.

    GALT's Belapectin prevented varices and decreased hepatic wedge pressures after only 12 months of therapy. That shows they loosened vascular resistance and portal hypertension caused by fibrosis.

    I'm sorry if you can't understand liver pathophysiology but can only think of fibrosis in a very" concrete"
    ( pardon the pun ) way.

    Fibrosis is dynamic, not static
  • S
    Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

    "Emerging evidence suggests that galectins, which are a 15-member family of evolutionarily conserved glycan-binding proteins, can act as endogenous modulators of neuroinflammation and potentially neurodegeneration [5, 6]. Among them, galectin-3 (Gal-3) is involved in cell adhesion, proliferation, migration, apoptosis, tumour progression, inflammation and innate and adaptative immune system modulation [7,8,9]."

    Gal-3 is a fascinating protein with a pleiotropic role in several physiological pathways. Numerous studies have shown that Gal-3 contributes to inflammation, microglial activation, remyelination, and neurodevelopment in neurodegenerative diseases. Major progress has been made in our comprehension of Gal-3 in the context of AD just a short time since the initial description of AD-associated Gal-3 abnormalities. This review summarizes Gal-3-induced microglia-mediated neuroinflammation in AD pathology. Clinical and experimental studies indicate that Gal-3 is crucial for the microglial response to the pathology of AD and that overexpression of Gal-3 may alter amyloid plaque aggregation and increase plaque-associated toxicity. The most prominent aspect of this molecule is that it can be successfully used as a risk marker of AD if measured in peripheral blood. The strong association of Gal-3 with the onset of AD and the prominent effects of Gal-3 on microglia in response to neuroinflammation suggest that Gal-3 inhibition for therapeutic purposes is an innovative and interesting strategy, although further clinical investigations are needed to clarify the potential for AD prevention."

    Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinf
    Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinf
  • A
    I agree with Larry.

    We need to prove the point in NASH first. But with a very favorable endpoint, the right dose and the right duration ( 18 months ) and the right entry stratification based on entry ELF scores, we have a good chance at success.

    I will assume that the extension cancer data will be good because the Cancer center would look very foolish publishing preclinical in Oncoimmunology, and then the clinical data in JITC and then following it up with new cancer data contradicting their prior publications.

    My feeling is that the company needs to open a third track in another discipline-such as Cardiology in Afib or cardiac fibrosis- partnering with an academic center and/or monetizing their patents.

    Eventually this platform technology will appear so overwhelming that a Big Pharma will gobble them up within the next 12-24 months.
  • A

    Just want to thank B for saving the day.

    Using his great spectrum of pharmacokinetics knowledge, including understanding of the concept of peak and trough drug levels, " B " has concluded that Belapectin is a safe drug, and when used in combination with Keytruda at the 4 mg/kg level it not only makes Keytruda more effective, but it reduces autoimmune toxicity.

    "B"'s analysis is in line with recent company press releases and with the most recent medical literature published in the Journal of Immunotherapy.

    On behalf of all shareholders, I thank you "B" for your astute analysis and contributions.
  • S
    When there are price dips, we get all this at a discount:
    Due Diligence Cliff's Notes from ST (updated):
    — Leading inhibitor under development for Galectin-3, key native immune system protein involved in numerous inflammatory and fibrotic diseases and various cancers.
    — The only drug that has ever shown any clinically meaningful (not just lab biomarker) benefit for NASH (prevention of varices), testing to repeat these results in the NASH-RX trial.
    — Appears to reduce the side effects of cancer immunotherapy in the MRK Keytruda combo trial.
    — Chiles Research Center published a paper in recent days in the #1 cancer immunotherapy journal JITC showing data that belapectin has positive effect in cancer patients.
    — Upcoming hepatic impairment (HI) biomarker results will guide the potential launch to additional indications.
    — Chairman and largest shareholder is the multi-billionaire founder/owner of ULINE. It’s his passion. His long time exec is now the GALT CEO and he has a board member from his family wealth office.
    — GALT CEO is taking 80% of his pay in the form of stock.
    — HC Wainwright raised Price Target from $12 to $14.
    — Multiple shots on goal include multiple indications + combo therapy possibility for each indication (drug has excellent safety profile).
    — BMY stated in a patent filed last year that the Gal3 inhibitor is proven to work for cancer immunotherapy. So we know that BMY is knowledgeable/ has their eyes on this.
    — Positive preclinical results for aOX40 cancer immunotherapy combo announced in recent days (this possible route is in addition to aPD-1 cancer combo and NASH).
    — Finished converting all preferred shares to common shares last year (historically, this is typically done for buy-in or buyout scenarios).
    — #1 on the fintel Short Squeeze Explorer as of 4/28, most likely to experience a short squeeze.
    — Richard Uihlein $10 million inside buy at $5 (convertible note), backing from a multi-billionaire.
    — Dr. Ben Carson joins the company!
  • A
    2021 Review:

    "This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodeling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis"

    My take:

    There is now over 10 years of data on Galectin 3 and heart disease ranging from atherosclerosis, to cardiac remodeling and cardiac fibrosis and numerous studies on Atrial fibrillation. This is ample evidence of causation and not simply correlation.

    Harvard clinicians have tried studies using Modified Citrus Pectin as the Gal3 inhibitor, ( essentially same method of action as Belapectin )- but it is simply impossible for any human being to ingest the right amount needed.

    The economic burden of Atrial fibrillation alone in the USA is 6 Billion/year, let alone all the other cardiac indications.

    Gal3 inhibitiors ? We are far ahead of competitors and we are safe

    If the posters here want to continue to fight the medical literature in NASH, cancer, cardiology, do it at your own peril.

    This is a platform technology.

    Very bright future ahead.
  • A
    From the April 27, 2021 Alzheimer's and Galectins article:

    "The extracellular biological activities of Gal-3 are mainly dependent on binding cell surface and extracellular matrix glycan-related ligands, such as laminin, MAC-2, collagen IV, fibronectin, Mac-2BP, and macrophage surface antigens [58]. These processes promote cell-to-cell and cell-to-matrix interactions, inflammatory responses, and cell development. The N-terminal domain of Gal-3 binds ligand (Bcl-2) and inhibits apoptosis [59]. Increased expression of Gal-3 in the extracellular space has already been verified in human diseases, including tumour development and progression and prognosis, neural degeneration and cardiovascular disease [60]."

    My take: EXTRACELLULAR Galectin 3 is what we need to target. That's where we have an advantage over small molecule inhibitors. We really stand alone ( and we also bind to the N terminal )
  • S
    May 6, 2021. “Most research in NASH is focused on the early stages of the disease, before it has progressed to cirrhosis. While this is certainly a very valid strategy, we should not forget those who have progressed to NASH cirrhosis, as their medical needs are the most pressing.”

    By Pol Boudes, M.D.
    By Pol Boudes, M.D.
  • A
    Galectin 3 is chimeric. It has two parts. The CRD ( carbohydrate recognition domain ) and the long N terminal.

    The role of the N terminal was always enigmatic. (Belapectin binds to the N terminal and somewhat to the CRD.)

    We always invoked allosteric inhibition of the CRD with Belapectin, but we no longer need to, as it is evident that the N terminal- where we bind- is crucial for Galectin 3 activity.

    The other companies with their small molecules ( Galecto, Glycomimetics, etc) all went after the CRD.

    Really a huge scientific paper in a very major scientific journal.
  • k
    With Merck's sales dragging from the pandemic and the company becoming increasingly reliant on immuno-oncology superstar Keytruda, the pharma giant's executive team unveiled a willingness to flex its M&A muscle.

    “We are open to any opportunity to add a meaningful asset,” president and soon-to-be CEO Rob Davis said on a Thursday call with investors. “We are open to all forms of deals and we have the capital” for those deals, he added.
    It'll soon have some extra cash on hand, too, thanks to the spinoff of Organon, which is expected to wrap up on June 2. Once the spinoff closes, Merck expects "to receive a special tax-free dividend of $9 billion, which we hope to deploy in a value-enhancing strategic business development opportunity," chief financial officer Caroline Litchfield said.

    The comments came during Merck’s first-quarter earnings call, where the drug giant reported sales for the period of $12.08 billion. Cancer mainstays Keytruda and Lynparza held the line, alongside surgery drug Bridion and the drugmaker’s animal health business.
  • A
    This is from the company's Dec 2020 press release regarding cancer combination and toxicity

    Chief Medical Officer Pol Boudes noted that relative to the Company’s cancer immunotherapy trial, “Our colleagues at Providence have already concluded that a phase 2 combination program where the combination of belapectin to Keytruda could be compared to Keytruda alone would be
    justified, first to confirm the efficacy of the combination but also to test the hypothesis on the reduction of auto-immune toxicities associated
    with PD-1 inhibitor monotherapy. We are currently evaluating the best options regarding the financing as well as the operational conduct of such a
    study that could identify an important advance for patients affected with these cancers.”
  • A
    'Topsy-turvy binding of negatively charged homogalacturonan oligosaccharides to galectin-3'
    Zheng Y., Su J., Miller M.C., et al Glycobiology volume 31 issue 3 pages 341-350 4/1/2021

    In this recent article in Glycobiology, sugars bind to the CRD in an upside down manner

    Looks like we bind both to the CRD and N terminal of Galectin 3.
  • S
    New in the Journal Nature:

    Anti-angiogenic agents — overcoming tumour endothelial cell anergy and improving immunotherapy outcomes

    "Endothelial expression of immuno-suppressive molecules. Various inhibitory molecules, expressed on endothelial cells of several tumour types, contribute to the endothelial immune cell barrier (FIG.1). One of these molecules is the carbohydrate- binding protein galectin 1, which is overexpressed in various malignancies and is a feature associated with poor prognosis. Galectin 1 facilitates tumour progression through its involvement in angiogenesis103 but also through its important role in suppressing immunity. Preclinical data indicate that, upon ligand interaction, galectin 1 expressed at sites of Tcell development and maturation can induce the apoptosis of activated Tcells, antagonize TCR- dependent signalling, inhibit the antigen- induced proliferation of Tcells and sensitize resting Tcells to FAS-mediated cell death. Galectin 1 is also overexpressed on tumour endothelial cells, resulting in limited infiltration by activated Tcells. Galectin 1 expressed by tumour cells also has an immunosuppressive role. In mouse models, the genetic silencing of galectin 1 in tumour cells resulted in enhanced antitumour immune activity. Nambiar etal. elegantly demonstrated that the secretion of galectin 1 by tumours can contribute to the endothelial immune cell barrier through the upregulation of PD- L1 and galectin 9 expression on the tumour endothelium, promoting immunotherapy resistance through Tcell exclusion. Accordingly, blockade of galectin 1 increased the infiltration of Tcells into the tumour, an approach that synergized with immune-checkpoint inhibition."

    Anti-angiogenic therapy has the capacity to ameliorate antitumour immunity and, thus, some combinations of anti-angiogenics and immunotherapies have been approved and a number of them are being tested. The authors of this Perspective describe how the
    Anti-angiogenic therapy has the capacity to ameliorate antitumour immunity and, thus, some combinations of anti-angiogenics and immunotherapies have been approved and a number of them are being tested. The authors of this Perspective describe how the
  • A
    It seems that the FDA is questioning ICPT's efficacy, safety, and the very data (liver biopsy) that they presented.

    This is as per ICPT longs posting on ST. They are in huge trouble, in my opinion.

    There are no other therapies for cirrhotics, and none on the horizon that I can see.

    Very unique opportunity here.

    Just my musings.
  • k
    Galectin-3 Is a Potential Mediator for Atherosclerosis

    There is strong evidence that Gal-3 participates in the initiation and progression of atherosclerosis. Numerous studies have shown that Gal-3 contributes to macrophage differentiation, foam cell formation, endothelial dysfunction, and VSMC proliferation and migration in atherosclerosis. In this review, we summarized several mechanisms pivotal to the development of atherosclerosis that are stimulated by local or circulating Gal-3. Amplification of cardiovascular inflammation and lipid accumulation in macrophage by Gal-3 are the most important mechanisms. Up to now, studies on Gal-3 have been focused on genetics and epidemiology suggesting that Gal-3 is positively related to the occurrence of atherosclerosis. Thus, Gal-3 can be regarded as a new biomarker for the risk evaluation of atherosclerosis and a new treatment target for atherosclerosis therapy. On the other hand, the application of Gal-3 inhibitors may be a potential treatment for atherosclerosis in the future. Moreover, macrophage plays a vital role in atherosclerosis, and some studies have indicated that Gal-3 can activate M2 macrophage differentiation, which has an anti-inflammatory property, through the CD98/phosphoinositide 3-kinase (PI3K) pathway [28, 99]. Activation of M2 macrophage differentiation by Gal-3 may be beneficial to the treatment of atherosclerosis through suppression of inflammation. As a key protein in autophagy progression, PI3K can be upregulated by Gal-3. Therefore, the augmentation of macrophage autophagy in atherosclerotic plaque through the Gal-3/PI3K/Akt/mTOR pathway is probably an effective therapy for atherosclerosis. To some extent, the multiple functions of Gal-3 depend on its N-terminal domain modification by matrix metalloproteinase (MMP). MMP-7 has been demonstrated to be a Gal-3 activator to exacerbate inflammation [100]. Hence, MMP can be regarded as a new target for further research on the connection between Gal-3 and atherosclerosis.
  • S
    Dr. Carson has a lot of media connections. We can easily hit $20+ with a little bit more increased mainstream investor awareness.

    Dr. Carson stated, “Galectin Therapeutics and its drug candidate, belapectin, are at the forefront of research into galectin inhibition, which appears to be implicated in many diseases, including NASH cirrhosis, which is a large unmet medical need. More broadly, early results and potential for belapectin’s use in combination with immunotherapy in cancer suggests belapectin could address a multitude of indications where galectin-3 is involved.
  • A
    Cancer cell International

    "Prognostic role of galectin-3 expression in patients with solid tumors"

    a meta-analysis of 36 eligible studies
    Wang Y., Liu S., Tian Y., et al Cancer Cell International volume 18 issue 1 pages 1-15 11/3/2018
    DOI: 10.1186/s12935-018-0668-y PMID: 30410421
    EISSN: 1475-2867 ISSN: 1475-2867

    Abstract Background Galectin-3 as a β-galactoside-binding protein, has been found to be involved in tumor cell growth, anti-apoptosis, adhesion, angiogenesis, invasion, and distant metastases, indicating that it may play a pivotal role in cancer development and progression. However, their results remain debatable and inconclusive. Hence, this meta-analysis was performed to clarify the precise predictive value of galectin-3 in various cancers. Methods PubMed, Web of Science, Embase, Cochrane Library, CNKI and Wanfang databases were searched comprehensively for eligible studies up to July 15, 2018. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) of OS or DFS/PFS/RFS were calculated to demonstrate their associations. Results A total of 36 relevant studies were ultimately enrolled in this meta-analysis. Our results shed light on the significant association of elevated galectin-3 expression with reduced OS or DFS/RFS/PFS in overall cancer patients (pooled HR = 1.79, 95% CI 1.42–2.27, I 2= 67.3%, p < 0.01; pooled HR = 1.57, 95% CI 1.04–2.37, I 2= 67.1%, p = 0.001). In tumor type subgroup analysis, we found high expression of galectin-3 was correlated with shorter OS or DFS/RFS/PFS in colorectal cancer (pooled HR = 3.05, 95% CI 2.13–4.35, I 2= 0.0%, p = 0.734; pooled HR = 2.49, 95% CI 1.82–3.41, I 2 = 0.0%, p = 0.738; respectively) and meanwhile it merely associated with reduced OS in ovarian cancer or non-small cell lung cancer (pooled HR = 2.24, 95% CI 1.38–3.64, I 2= 0.0%, p = 0.910; pooled HR = 2.07, 95% CI 1.48–2.88, I 2= 0.0%, p = 0.563; separately).
    Conclusions Taken together, our results suggested that galectin-3 played an oncogenic role in colorectal cancer, ovarian cancer and non-small cell lung cancer, indicating it could be a promising biomarker and a novel therapeutic target for them. Further studies were warranted to validate our findings.
  • S
    According to the paper in JITC (#1 cancer immunotherapy journal) published just a few weeks ago:

    "In summary, these data demonstrate that belapectin+pembrolizumab therapy is safe, associated with increased T-cell activation, limited expansion of M-MDSCs, and favorable clinical responses."

    Enhancing clinical and immunological effects of anti-PD-1 with belapectin, a galectin-3 inhibitor


    "IS SAFE" Huge Advantage for GALT belapectin!
  • A
    There is no drug that can treat late stage NASH fibrosis/early cirrhosis. We stand alone. Market does not realize this just yet
  • A
    One day these guys are short, next day they are long.

    New line now -- " chasing a wet dream " has replaced "fantasy investing"

    They always win, they never lose.

    It's comical.

    The only reason I care is that the guys who spread fear and uncertainty dissuade the little guy investor from obtaining knowledge. I am not worried about the company's money situation with their multibillionaire COB.

    We are posting significant knowledge on Galectin 3 and Gal 3 inhibition for the small investor to beat Wall Street. That's why we are taking time and effort here.

    As far as whether or not this works- there is no ample evidence in preclinical cancer and NASH models that this works, plus posthoc clinical analysis in NASH that it prevents esophageal varices, and now clinical evidence in cancer that Belapectin increases ICI (immune checkpoint inhibitors) effectiveness and it decreases ICI autoimmune toxicity.

    More cancer data is coming.

    For the small investor out there this remains a highly speculative investment with a tremendous reward potential. The drug is a potential platform technology for many diseases. I see a very bright future ahead.

    I might be wrong.

    Do your own DD. Never trust anyone on these boards.