While user B is trying to spread unscientific misinformation regarding binding, coincidentally this new paper was published today with a concise explanation of the complex and subtle allosteric modulation of glycoprotein interactions. This is consistent with the other papers I posted previously. Never take the word of some anonymous message board poster without checking sources. Disgusting how some people try to spread misinformation in order to short stocks. It's even more mortally repugnant when this involves medical stocks."Born to be boundThe main biological function associated to glycoproteins is molecular recognition. Glycoproteins inherently target (or belong to) all kinds of cellular receptors to mediate responses in signal transduction, inflammation or intracellular communication. Molecular determinants of such interactions have been extensively characterized for years by studying the interaction between the isolated glycan and its natural protein receptor [65,66], but the use of entire glycoproteins for such studies is only now emerging. This is very relevant because the glycan is not a mere transducer of the intermolecular interaction, but it can also alter the conformational ensemble of the protein, as determined by NMR spectroscopy in the mucin's glycopeptide MUC1 [67•]. In another elegant example, N-glycosylation of the IgG1 Fcg receptor is mandatory for binding its receptor, even though the carbohydrate does not participate in direct interactions. Instead, motions in the N-glycan allosterically modulate the affinity for the receptor, a mechanism that has been demonstrated computationally [68] and experimentally by NMR linewidth analysis [69]. Such motions are also transmitted to the IgG1 Fc fragment, particularly to a cluster of amino acids (Gln295-Thr299) that experience chemical shift perturbation upon N-glycosylation in position Asn297 [70]. Alternatively, anchoring the glycan to the protein may restrict the conformational space explored by the glycan, which has a direct consequence on glycan presentation and interaction with receptors. For instance, glycoprotein characterization and interaction studies by NMR were combined with MD simulations to provide with a structural model of the FcεRIα glycoprotein and its interaction with the carbohydrate recognition domain of the human galectin 3 [42••].The show must go onIn summary, solution NMR characterization of glycoproteins is most rewarding since the interaction between the carbohydrate moiety and the polypeptide is unexpectedly complex and subtle, often unraveling allosteric effects and conformational ensembles that embed the functional conformations."NMR of glycoproteins: profiling, structure, conformation and interactionshttps://www.sciencedirect.com/science/article/pii/S0959440X20301561

I noticed that Galecto (GLTO) IPO'd today.A mkt cap of $85mm.A little baby GALT.......LOLActually GALT mkt cap is only twice as high.Grossly undervaluedI strongly believe that GALT will be announcing Providence next week.With positive results.After that announcement,mgmt may announce business update.IF Providence is announced w/ positive results...........everything points to a double digit stock in Nov.In the teens.One last thought.........When the pps broke hard thru the bollinger bands in late Sept....but pps settled back at the same starting price,that is a textbook example of future potential explosive pps growth.IMO,GALT is getting ready to run.Hope all have a good weekend

Nice NASH drug review just published. GALT drug listed as the ONLY antifibrotic therapy in late NASH trials. See ST.

I wish I had another finger so I could give this three thumbs down

New study by AstraZeneca and scientists in Sweden and UK finds that galectin-3 has a key role in myocardial infarction (heart attack) inflammation:“Identification of driver genes in MI.Lgals3 (encodes galectin-3) and Prkaca were among the most central genes in central clusters (Table S6).”Lgals3, related to acute inflammation response, has been studied intensively in recent years as a key gene in CVD, and as a potential CVD therapy target (Suthahar et al., 2018; Zhong et al., 2019).”Revealing tissue-specific metabolic crosstalk after a myocardial infarctionhttps://www.biorxiv.org/content/10.1101/2020.10.28.358556v1

The other issue here is a monosaccharide delivery via the gut. Lactose is a disaccharide ( Glucose-Galactose) and binds very well to the Gal 3 CRD, but just releases very quickly.In a disease now felt to be related to the gut microbiome, a sugar delivered orally via the Gut is counterintuitive- might fuel the fires of the gut microbiome.I like GALT IV delivery.

So let's think about this. Jan 2020 - TD 139 was rapidly excreted- no good , but the monosaccharide GB 1107 has prolonged half life. How are they going to deliver this? (I think they are working on a piggy back carrier molecule, not sure).Very far behind, many, many years

Agree, more eyes on Gal 3 inhibition, the better. GLTO has drug delivery issues, and is preclinical for NASH

Jan 2020In Vivo Veritas: 18 F-Radiolabeled Glycomimetics Allow Insights into the Pharmacological Fate of Galectin-3 InhibitorsKlas Bratteby 1 2 3 4, Edvard Torkelsson 2 3, Elina Tampio L'Estrade 1 2 5, Kristoffer Peterson 3, Vladimir Shalgunov 1 4 5, Mengfei Xiong 1 5, Hakon Leffler 6, Fredrik R Zetterberg 7, Tomas G Olsson 2, Nic Gillings 4, Ulf J Nilsson 3, Matthias M Herth 1 4, Maria Erlandsson 2Affiliations expandPMID: 31846326 DOI: 10.1021/acs.jmedchem.9b01692AbstractGlycomimetic drugs have attracted increasing interest as unique targeting vectors or surrogates for endogenous biomolecules. However, it is generally difficult to determine the in vivo pharmacokinetic profile of these compounds. In this work, two galectin-3 inhibitors were radiolabeled with fluorine-18 and used as surrogate PET tracers of TD139 and GB1107. Both compounds are promising drugs for clinical applications. In vivo evaluation revealed that both surrogates strongly differed with respect to their biodistribution profile. The disaccharide (TD139 surrogate) was rapidly eliminated from blood while the monosaccharide (GB1107 surrogate) showed no sign of excretion. The data obtained allowed us to infer the different in vivo fate of TD139 and GB1107 and rationalize how different administration routes could boost efficacy. Whereas the fast excretion profile of the TD139 surrogate indicated that systemic application of disaccharides is unfavorable, the extended biological half-life of the GB1107 surrogate indicated that systemic administration is possible for monosaccharides.We have both Pk and drug delivery issues with Galecto. This is the latest data- 2020

Definately will not have to wait till 2023/24 for fibrosis results we will move off of this data one way or another...."Its lead product candidate, GB0139, is an inhaled inhibitor of galectin-3 for the treatment of severe fibrotic lung diseases such as idiopathic pulmonary fibrosis (IPF). The company has conducted a Phase 2a trial in 24 IPF patients and has initiated a Phase 2b trial in 450 IPF patients, with topline results expected in 2022."

Galecto (GLTO) Prices mid point @ 15.00 BofA, Leerink, CSFBNot a bad group of underwriters two majors and a well respected boutique that deals in the space.Deal was not substantially oversubscribed or it would have priced at or above the high end of the range (14 to 16)It is important to us that this deal does not crater Valuation wise they are at 220 million plus cash of 115 or so.. If they pop the deal or run with support in the aftermarket people will start to look at competitors.If the deal falls apart it will not bode well for our capital raise.should be an interesting day

Galecto was ranked 0-.50 cents a basically flat expectation from those that would flip the dealDo it as a courtesy to your broker type event.That's where it opens and trades up slightly, plus .30 cents on what is really very little volume. To me that means deal is placed well which infers interest in Galectin three inhibition from investment community. More eyes on space, thats good, a valuation premium to ours holding up in the open market is good news as well.

Technically,this chart is looking great.If Providence is to be positively announced,I am in agreement with an earlier statement by Anonymous.It will be announced separately from E/R update and by looks of this chart,I am guessing next week.IF that is correct,it would give GALT more exposure to potential investors by being announced and covering the subject twice.This is not an attempted pump by me.Just expressing my view.

nice premarket , lets go with mln volume

Pancreatic cancer (PDA) is one of the most difficult cancers which rarely responds to any therapies, so big pharma is very interested in combo treatments that can make immunotherapy work for pancreatic cancer. In this major new study published today in the journal Nature, galectins are recognized as pancreatic cancer checkpoints. Currently approved checkpoint inhibitors target the molecules CTLA4 and PD-1. GALT GR-MD-02 (belapectin) inhibits LGALS9 (Galectin-9) in addition to Galectin-3. The previous GALT phase 1 cancer combo results found that responding patients had "a significant decrease in the frequency of suppressive myeloid-derived suppressor cells (MDSC) following treatment in the responding patients." In the new study,"The expression of checkpoint ligands was heterogeneous, with epithelial cells mainly expressing PVR and LGALS9 (encoding for PVR and GALECTIN 9, ligands for TIGIT and HAVCR2 (TIM3), respectively). Myeloid and dendritic cells expressed several genes encoding checkpoint ligands, including SIRPA, LGALS9, PVR and ICOSLG (Fig. 2c)."Multimodal mapping of the tumor and peripheral blood immune landscape in human pancreatic cancerhttps://www.nature.com/articles/s43018-020-00121-4

Next 8 weeks might be interesting with expected cancer data.But immediately, the Galecto IPO might give us a sense of how the market values Gal3 inhibitors.Don't worry, Galecto is preclinical for NASH and continues to struggle with a delivery system.As far as Galmed, the mechanism of action is via SCD1, which then turns on PPAR gamma, once again a very indirect antifibrotic MoA, and I don't see any good proof of PPAR gamma antifibrotic activity.Of course, our resident clown will say that there is no proof of GALT antifibrosis. He continues to lack any understanding of the dynamic effects of fibrosis on portal vasculature resistance and thinks that we just look at collagen staining on a slide to understand fibrosis and its effects.The latest Scripps article showing live cell mapping detailing the macrophage - HSC link and activation via Gal 3 should help him understand

Valuation potentials50,000,000 potential fibrosis and cancer patients 1,000 per regime is 50 billion in revenue10,000 per regime is 500 billion in revenueMaybe you get 30 percent of market in the us alone that is a 50 to 100 billion dollar price tag upon a significant level of commercialization at the 1,000 dollar price point.50 billion divided by 70 million is 700.00 per share.we will never see that... but some big pharma guy will do the math and the 10 billion they pay you in 2023 will not seem that offensive to its long term shareholders.I woukd be surprised if a regime costs only 1000 dollars but pricing if the government where to get involved could become stupid in a hurry.The potential is awesome for sure.

Someone on stocktwits just posted that Galecto IPO is coming 15.00 per share 332.00 Market capIPF candidate phase 2/bthis is a galectin three inhibitor they have both oral and inhaled versions In general they are pursuing our market and have early investments from MERK and BMY.....Heyyy look out here comes the hare....if they can do this deal at 332 million we should get a pop out of that.Think about it like this as well La Jolla de risked for you the Kidney fibrosisGalecto will de risk the lungs.We will do the liver and hopefully the heart.That is incredibly valuable information to have, demonstrated efficacy in two years time for three fibrotic indications. Galecto maybe a competitor but this is a huge market and lots of suitors.Cancer comes up roses and it really will be a good year for shareholders next year

What if providence just never quits enrolling patients.If data is good why not continue to serve the patients and enroll new ones implement a phase 2/3 on the fly as per say. Why break down the recruitment effort then have to rebuild that? Why shouldn't this wave of patients be extended the opportunity to continue, shouldn't that be how it works. Did 1st Phase one recipients go on receiving therapy after trial was officially over? What is the impact of that on peoples lives?The 22 patients in this phase one 4 mg cohort should be the leading edge of our phase 2/3 study.if you will, continue to recruit patients under this expansion of phase one.If there is enough evidence to go forward clinically, if there are no inclusion/exclusion type issues. Can we not recruit and enroll throughout the trial design and protocol submission process which should really only be changing length of study?That would be a real confidence builder....

Current market cap vs potential market cap = opportunity This best in class in biotech universe that I know ofWhy i am here. Maybe should not even be public at this stage but it is..... That's the real advantage of the investor that does its research in the public domain.Comprehension of potential value is hard to get your head wrapped around, Its googlish to think about it, but it is very real in this stock.Retirement stock is an appropriate sentimentscience proving God willing