Esperion Therapeutics Inc (ESPR)

[FACT-MASTER]

Looks like Esperion's new ACLY inhibitor program has a patent application in progress:


"Macrocyclic inhibitors of atp citrate lyase"

https://patentscope.wipo.int/search/en/WO2025096751

Published May 8/25

[Gregg4]

We have a pulse ladies and gentlemen I'm still here buying

[FACT-MASTER]

I don't see the triple combo trial on Esperion's pipeline website anymore. I know it was there along with Nexlizet and Nexletol recently.

Now, nothing regarding BA

https://www.esperion.com/science/pipeline

Not in communication with Brinks, the DS/DSE buyout idea is a result of logic and due diligence.

DSE conducting the trial, no mention of ESPR here:

https://clinicaltrials.gov/study/NCT06686615?term=Daiichi%20Sankyo%20Europe&rank=10&a=3&b=5

[Gregg4]

That's from Brinks and he's full of shit as always but I hope it true

[FACT-MASTER]

Speculation: DSE has either bought the entire company of Esperion OR just the rights to BA. - just my opinion and time will tell.

[FACT-MASTER]

ESPR: link to DSE study

https://clinicaltrials.gov/study/NCT06686615?term=Daiichi%20Sankyo%20Europe&rank=10&a=3&b=5

Link to completed PCSK9 study

https://clinicaltrials.gov/study/NCT03193047?term=esperion&page=1&rank=6

[FACT-MASTER]

What happened to the "triple combo development items" on Esperion's PIPELINE web page?

https://www.esperion.com/science/pipeline

[FACT-MASTER]

Here is the study on clinicaltrials.gov

https://clinicaltrials.gov/study/NCT06742853

[FACT-MASTER]

Gregg,

Do we know that Astra Zeneca currently has a triple combo trial in progress including a cohort of Bempedoic Acid/Ezetimibe/ and their AZD0780 ( AZD0780 is an investigational once-daily oral PCSK9 inhibitor for patients currently not reaching their LDL-C lowering goal despite standard-of-care lipid-lowering therapies such as statins)

https://www.astrazenecaclinicaltrials.com/study/D7960C00017/
(if this hasn't been posted, please post on st)

Study Start Date: 20 Dec 2024
Estimated Primary Completion Date: 04 Dec 2025
Estimated Study Completion Date: 04 Dec 2025

Also, a recent publication on AZD0780:
https://www.appliedclinicaltrialsonline.com/view/pcsk9-inhibitor-ldl-cholesterol
and video:
https://clinicaltrialresults.org/dr-michael-j-koren-and-dr-c-michael-gibson-discuss-efficacy-and-safety-of-azd0780-an-oral-small-molecule-pcsk9-inhibitor-for-treatment-of-hypercholesterolemia-results-from-a-ph2b-randomized-plac/

[FACT-MASTER]

( i might have that all wrong, hdl might increase after discontinuation of BA and Fenofibrate)

I haven't read the study and might be suffering from a case of ESPR hopium, i need a drink)

[FACT-MASTER]

Also, the NEJM posted a chart on their X site ( no doubt from the study)

Correspondence: Severe HDL Cholesterol Reduction with Bempedoic Acid and Fenofibrate https://t.co/8L4mLxC1nM #Cardiology #Genetics pic.twitter.com/B2A3UciCwQ

— NEJM (@NEJM) April 2, 2025

WOW!, imo.

ApoA-I: The primary protein component of high-density lipoproteins (HDLs), which are often considered "good" cholesterol, and plays a role in cholesterol transport.

( the title of the study is somewhat confusing, you have to look to the Abstract preview to see that it is bempedoic acid that appears to activate a severe increase in HDL )
"Abstract
A reversible interaction between bempedoic acid and fenofibrate leading to a major, reversible decrease in HDL cholesterol levels was found in patients treated for nongenetic elevated LDL cholesterol levels."
https://www.nejm.org/doi/full/10.1056/NEJMc2413726

[FACT-MASTER]

Can you post this reference on st, to a study that was done with BA and Fenofibrate ( AbbVie Inc.)
Possibly some posters there subscribe to the New England Journal of Medicine and can access the publication.

https://www.nejm.org/doi/full/10.1056/NEJMc2413726

( has this study been posted on st before?, i don't recall seeing this study posted)

Study dated March 26,2025, so very new, and appears to reference bempedoic acid with activating a severe increase in HDL.

Why would this be important?

HDL, also known as high-density lipoprotein, is a type of cholesterol that is considered "good" cholesterol because it helps remove excess cholesterol from the body and can lower the risk of heart disease. HDL is transported in the bloodstream by proteins called lipoproteins, and it's crucial for maintaining overall heart health.
Here's a more detailed explanation:
What is HDL?
HDL is a type of lipoprotein that circulates in the blood and helps transport cholesterol, a type of fat, throughout the body.
Why is it called "good" cholesterol?
HDL helps remove excess cholesterol from the bloodstream and carries it back to the liver, where it can be processed and eliminated.
How does HDL protect against heart disease?
High HDL levels are associated with a lower risk of heart disease, stroke, and other cardiovascular problems.
How to increase HDL levels:
There are several lifestyle changes that can help increase HDL levels, including exercise, following a healthy diet rich in fruits, vegetables, and whole grains, and avoiding smoking.
Healthy HDL levels:
For men, a healthy HDL level is generally considered to be 40 mg/dL or higher, while for women, it's 50 mg/dL or higher.
HDL and reverse cholesterol transport:
HDL is responsible for reverse cholesterol transport, which is the process of transporting cholesterol back to the liver for processing and elimination.

[Gregg4]

I'm holding on by a string

[FACT-MASTER]

Tolvaptan/BA study (ESPR funded)

https://www.frontiersin.org/journals/molecular-biosciences/articles/10.3389/fmolb.2022.1001941/full

Now that's MEGA!!

[FACT-MASTER]

Gregg, how are you?

We need to start a MEGA (Make Esperion Great Again) movement.

RH makes some good points, imo

[FACT-MASTER]

Although the recent R&D day alludes to a "new" molecule for development, it should be noted that BA on it's own merit is imo, already a "platform" for possible further licensing for liver disease conditions. Take a look at these studies and hope you concur that BA has more potential then just hyperlipidemia.
( feel free to hit st with all studies, lol)

https://pmc.ncbi.nlm.nih.gov/articles/PMC8663992/

https://pubmed.ncbi.nlm.nih.gov/34887111/

https://pmc.ncbi.nlm.nih.gov/articles/PMC9312949/

https://pmc.ncbi.nlm.nih.gov/articles/PMC9820553/
(potential inhibition of the mTORC1-S6K1 pathway)

https://pubmed.ncbi.nlm.nih.gov/37684055/

https://dmd.aspetjournals.org/article/S0090-9556(24)01100-0/abstract

These studies are particularly on liver conditions ( i know the guys on st have mentioned kidney, parkinson's maybe a few others which i concur has further BA licensing possibilities), however i bring attention to the fatty liver conditions particularly due to Novo's SNDA in progress, and wonder why there is no collaboration with Novo on their GLP-1 SNDA for MASH study with the addition of BA.
Esperion, imo could just as easily be taking the route of a SNDA for various liver conditions. ( a buyout by novo would of course answer these questions, however we are no where near a buyout price - it's a perplexing situation, imo.)
Novo's study as recently posted:
https://www.prnewswire.com/news-releases/essence-phase-3-trial-of-semaglutide-showed-significant-improvements-at-72-weeks-in-adults-with-mash-published-in-nejm-302443359.html

[FACT-MASTER]

https://link.springer.com/article/10.1007/d43592-025-00002-x?gad_source=1&gad_campaignid=22387166154&gclid=Cj0KCQjwlMfABhCWARIsADGXdy_LvYRrm-ecz15O9u4n2O2qK1iyBqJfhpJiK2eHJa4vH8ErUAmfLr8aAh9yEALw_wcB

I guess AstraZeneca hasn't heard of Esperion or bempodeic acid either.

[FACT-MASTER]

https://www.prnewswire.com/news-releases/essence-phase-3-trial-of-semaglutide-showed-significant-improvements-at-72-weeks-in-adults-with-mash-published-in-nejm-302443359.html

I guess "no interest" from Novo on the GLP-1/BA combo even though this study demonstrated the combo improved various parameters.and reduced fibrosis.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10518624/

Nothing appears to be working in ESPR's favour

[FACT-MASTER]

R&D Day appears to be have been informative on Esperion's next gen ACLY inhibitory strategy targetting various diseases.
All sounds logical with highly credible presenters, Sheldon speaks well on the business side of things as well ,imo. However, isn't it time now, to implement a strategy for ESPR shareholders to see the stock price rise to a minimum of $5.00? ( or is that asking too much, it seems like $1 will be a milestone event, and imagine the rejoicing if we hit a whole $2.50?).

One thing i am quite confident about is that Pinkosky ,Mantzoros amd Cohen - it desn't matter "who" they work for, their life is their research, so if they are working for DS / Eli-Lilly / Merck - it's all the same for them. Would they like a little ( or alot ) $$ in their bank accounts from an ESPR buyout - I'm sure they would.

[FACT-MASTER]

ESPR R&D Day April 24/25 Video

Nice informative R&D Day Esperion - looks like a nice get together in NY,NY.
Guys, did you notice the stock price is at .90?

Yeah, i get it, mechanism starting with ACLY inhibition and then targetting the indication.

Excellent presentations from all, particularly liked the guy from Greece and Poland.

Sale of rights to BA a strong possibility, imo. =DS

[FACT-MASTER]

Looks like Eli and Takeda active in addressing PSC:

https://patents.google.com/patent/EP3866806A1/en

https://patents.google.com/patent/US20210388092A1/en

i can actually now see clearly that a sale of Esperion's BA franchise (rights to BA and all things BA) is a strong possibility with DS being the #1 possible suitor for that, possibly 1 billion and change for the BA rights, ESPR continues with developnment of the "next gen ACLY inhibitor".

I'm not optimistic here, it's been a deadend for longterm shareholders irregardless of all the due diligence /scenarios, the guys on st do and come up with

[FACT-MASTER]

Merck has a couple of informative sites on PSC, as a point of information


https://www.merckmanuals.com/en-ca/professional/multimedia/video/overview-of-primary-sclerosing-cholangitis-psc

https://www.msdmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/sclerosing-cholangitis

[FACT-MASTER]

I concur with Bear on the "ACLY inhibitor platform" angle, however where is the IP for such a platform which would include the "next generation ACLY inhibitor" and indication for PSC.

This new angle may or may not be related to BA, there was nothing stated in the press release that the new lead candidate was BA or related to BA.
( so what are they going to do with the BA/GLP-1 study - just shelve that? - nothing makes sense).
Information is missing, imo, however i have not listened to the presentation yet.

EXCERPT1

Target validation underpins Esperion’s next-generation ACLY inhibition discovery program in liver diseases.


Selected PSC as the lead indication for next-generation ACLY inhibition discovery program.

Utilized multi-omics, phenome-wide association studies, and preclinical disease modeling to uncover novel ACLY pathways and disease links beyond cardiovascular disease.

Identified ACLY mechanisms linked to bile duct injury, inflammation, and fibrosis – key drivers of PSC progression.


Progressing a differentiated ACLY inhibitor program with strong preclinical data.


Discovered lead candidates through high-throughput and structure-based screening, optimized for PSC-specific biology.

Observed efficacy in human liver microtissues, and chemically and surgery induced liver injury models.

Showed consistent reductions in liver injury, inflammation, and fibrosis across multiple preclinical models.


PSC represents a large unmet medical need with no approved therapies and significant market potential.


Potential eligibility for Orphan Drug and Fast Track designations from the U.S. Food and Drug Administration.

Estimated >$1 billion annual market opportunity.

Estimated prevalence of approximately 76,000 diagnosed PSC patients across the U.S. and Europe as of 2024.

[FACT-MASTER]

ESPR: Esperion Unveils Promising Research Supporting Lead Development Candidates for Primary Sclerosing Cholangitis (PSC) at R&D Day 2025

https://stocktwits.com/symbol/ESPR

[Gregg4]

Same as us baffled

[FACT-MASTER]

Hard to understand what is going on here with ESPR stock.

Does Gary have any insight?

Thank you,
FM

[Monksdream]

ESPR, new 52 week low

[Gregg4]

Yes really good stuff excellent research 

[FACT-MASTER]

Thanks for posting on st, some good responses.

Today's posts from Bear and meistermell i found very interesting, although not direct responses, their posts are more directed to the "next steps" beyond having the IP / claims / descriptions etc. for BA/GLP-1 combo in place. From their posts today, it sounds like there has been more pre-clinical work done that most are unaware of.

I would hypothesize as well that a sNDA ( supplemental New Drug Application) application is a strong possibility as well, since in this instance both BA + GLP-1 are already FDA approved for their respective indications. If the sNDA were possible, that could significantly reduce the timeline for approval of a new indication, in this instance a new liver indication. Article here on Supplemental Drug Approval Process - however it's a bit old, but i see a nice example of Darzalex from Dr. McKee getiing a second approval in 1 year and a third in another 7 months after the intial FDA approval.
https://ascopost.com/issues/december-25-2017/fda-helps-streamline-approval-process-for-supplemental-drug-indications/

Anyways, that's as far as i will go on hypothesis, the new indication has many angles it could go, best to just wait and see what SK has to say on R&D day.
Would be huge to see Eli-Lilly take an equity stake in ESPR via offering, say 15 million shares at $5.00/share.- i'm probably dreaming here on a Sunday afternoon. (lol)

[FACT-MASTER]

ESPR April 18/25: FORM S-3 REGISTRATION STATEMENT UNDER THE SECURITIES ACT OF 1933.

https://www.sec.gov/Archives/edgar/data/1434868/000110465925036348/tm2512507-1_s3.htm

EXCERPT1

"The information discussed above is illustrative only and will adjust based on the actual public offering price and other terms of this offering determined at pricing.
The table and discussion above are based on 197,846,661 shares of our common stock outstanding as of December 31, 2024. The number of shares outstanding as of December 31, 2024 excludes:

• 5,177,511 shares of our common stock issuable upon the exercise of stock options outstanding as of December 31, 2024, at a weighted average exercise price of $8.70 per share as of such date;

• 632,950 shares of our common stock issuable upon the exercise and achievement of the performance criteria of our performance-based stock options outstanding as of December 31, 2024, at a weighted average exercise price of $4.97 per share as of such date;

• 4,447,074 shares of our common stock issuable upon the vesting of restricted stock units;

• 6,389,494 shares of our common stock reserved for future issuance under our 2020 Employee Stock Purchase Plan, as amended, as of December 31, 2024;

• 1,167,707 shares of our common stock reserved for future issuance under our Amended and Restated 2013 Stock Option and Incentive Plan and our 2017 Inducement Equity Plan, as amended, as of December 31, 2024; and

• 26,071,429 shares of our common stock issuable upon the exercise of outstanding warrants.

To the extent that any options are exercised, new options are issued under our 2022 Stock Option and Incentive Plan, as amended, and our 2017 Inducement Equity Plan as of December 31, 2022, or we otherwise issue additional shares of common stock in the future (including shares issued in connection with acquisitions), there will be further dilution to new investors.
In addition, we may choose to raise additional capital due to market conditions or strategic considerations, even if we believe we have sufficient funds for our current or future operating plans. To the extent that additional capital is raised through the sale of equity or convertible debt securities, the issuance of these securities could result in further dilution to our stockholders."

[FACT-MASTER]

EXCERPT 3

"[0301] Perhaps most importantly, in this study, it was found that combining bempedoic acid with liraglutide resulted in reductions in fibrosis. These pathological findings were supported by transcriptome data indicating combination therapy reduced extracellular matrix synthesis, epithelial-to-mesenchymal transition, myofibroblast regulation, focal adhesion kinase, and collagen biosynthesis and modification. This is of great importance as, to date, neither liraglutide or semaglutide have shown efficacy at reducing fibrosis stage in patients with NASH. Furthermore, the analyses revealed that a potentially unique effect of bempedoic acid may be due to its effects on countering Lira-induced increases in the TGF-R activated transcription factor Smad3, which is a critical driver of fibrosis. (Schwabe et al.; Mechanisms of Fibrosis Development in Nonalcoholic Steatohepatitis .; Gastroenterology [Internet]. 2020;158(7): 1913-28.) As the GLP-1R is not expressed on hepatic stellate cells (Yabut and Drucker.; Glucagon-like Peptide-1 Receptor-based Therapeutics for Metabolic Liver Disease. Endocr Rev."

[FACT-MASTER]

EXCERPT 2

"[0294] Hepatic stellate cells are critical for driving liver fibrosis and therefore the expression of key markers implicated in NASH progression were explored. (Payen et al. ; Single-cell RNA sequencing of human liver reveals hepatic stellate cell heterogeneity.', JHEP Reports [Internet].; 2021; 3(3): 100278.) Consistently, markers of activated stellate cells (Collal, Colla2, ColSal, Lox, Timpl ) were significantly reduced in the Lira+BemA treatment groups to a greater extent than monotherapies of Lira or BemA (FIG. 3D). Interestingly, BemA appeared to counteract Lira-induced upregulation of TGFP effectors, including Smad3, a transcription factor critical for upregulating fibrotic pathways in NASH (FIG. 8B). Moreover, combination therapy generally reduced the expression of several chemokines implicated in NASH progression greater than Lira or BemA treatment alone (FIG. 3E). Collectively, these data indicate that combination therapy with Lira+BemA induces an anti-fibrotic and anti-inflammatory gene-expression profile that is predictive of reduced liver pathology (steatosis, ballooning, and fibrosis).

Combination Treatment Induces a Prognostically Favorable Gene Expression Profile That Most Closely Resembles Those from Healthy Human Liver Biopsies

[0295] In humans a 25-gene signature has been established to be predictive of NASH severity (Govaere et al. 2020). Therefore, to contextualize the clinical significance of the experimental therapies, an integrative analysis combining the expression data of 22 orthologous genes derived from the treatment cohorts with the expression data derived from 216 NAFLD/NASH patients was performed. Combination treatment significantly downregulated the expression of 13 genes in this prognostic signature. Hierarchical clustering using Pearson correlation reveals four clusters with differential compositions of healthy individuals, patients with pre-fibrotic (NAFLD, F0-F1) or fibrotic (F2-F4) disease and the experimental cohorts (FIG. 4A). Cluster II exhibits the most clinically benign phenotype. 80% of healthy individuals in the patient derived dataset are represented in this cluster compared to 7.55%, 1.85% and 0% of patients with F2, F3 and F4 stages of disease (FIG. 4B). It was found that 4 out of 6 of the combination treatment samples colocalized in this cluster while monotherapy treatment samples are mostly grouped in clusters I and II which exhibit more advanced disease. Using PCA, the progressive resolution of NASH in human patients on PCI is shown (FIG. 4C). Mapping the control, monotherapy, and combination treatment cohorts with human NASH disease stages further supports the increased

transcriptional similarity between healthy individuals and combination treatment samples beyond what can be achieved using Lira and BemA alone."

https://patentscope.wipo.int/search/en/WO2025014754

[FACT-MASTER]

Here is some weekend study material for the ST board:

https://patentscope.wipo.int/search/en/WO2025014754

Click on "DESCRIPTION" and "CLAIMS"

EXCERPT1

"5. A method of reducing the body weight of a subject with hepatic steatosis, the method comprising administering to the subject an effective amount of a GLP-1 receptor agonist and an effective amount of bempedoic acid."

Your welcome,
FM

[FACT-MASTER]

Is an Eli-Lilly collaboration possible, come April 24/25?

https://www.statnews.com/2024/06/05/eli-lilly-mash-zepbound-tirzepatide-liver/

https://www.cnbc.com/2024/02/06/eli-lilly-weight-loss-drug-may-treat-fatty-liver-disease.html

Don't forget Eli-Lilly was mentioned in this study:

https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(23)00360-9

and Esperion is the owner of this patent:

https://patentscope.wipo.int/search/en/WO2025014754

Should we be optimistic for April 24/25? - let me know what your "wingman" thinks. Thanks

[FACT-MASTER]

ESPR: April 2025 Corporate Presentation

https://www.esperion.com/static-files/a59ef921-0969-487f-98c6-de85c5c57cc6

Nice presentation.

Slide 18 pipeline "hepatic disease" = could be a wide variety of liver conditions.

Nice write up here on liver/liver conditions

https://www.webmd.com/fatty-liver-disease/liver-and-hepatic-diseases

EXCERPT1

"Liver Disease FAQs
What are common diseases of the liver?

MASLD, cirrhosis, and hepatitis.

What are the first signs of a bad liver?

Early liver disease doesn’t usually cause any symptoms. If you notice that the whites of your eyes or you skin are starting to look yellow, there may be something wrong with your liver.

What are the most serious liver diseases?

All liver diseases are serious, but cirrhosis is quite serious. Once the liver gets scars, it can’t work properly.

What is the first stage of liver disease?

The first stage of liver disease is fatty liver disease. This is when you get fat inside the liver."

[Gregg4]

I don't see it that way maybe I'm delusional🤣 But it has been hanging here way too long should've bounced, i've also seen too many times where I've left my wingman too early but it's been 4 years

[FACT-MASTER]

Level II ask stacked as far as the eye can see!

Looks like dilution on the way, no way out of this - we going down.

Can only think of one reason for that - some sort of acquisition.

We being the dumbasses holding all the worthless paper ESPR shares.

Seen this story all too aften, everybody talking about the great opportunity to "buy more". There is no way "wall street" would miss an opportunity like this, this is a failure on a macro scale and just a matter of time now before the ship sinks out of sight, - suspect dilution for acquisition with R/S later this year, imo. Sorry for the negative bro, just calling it the way i see it - no way out of ESPR without a loss.
Holding and will go down with ship - ouch.
Wasatch - wow!

[Monksdream]

ESPR under $2

[PonkenPlonken]

good for nothing

[Gregg4]

Brinks reached out to me wanted to get in touch with you?

[PonkenPlonken]

Why is there an AI LDL-C minion in the newest presentation on slide 12?
Anyways looks much better than previous one. They keep talking about these dreams of sudden massive adoption due to heightened awareness.
Its not going to happen and if it were to happen it would likely be due to a new drug that has a very attractive regimen... maybe one thats one and done.

[Gregg4]

Yup agree not helping

[FACT-MASTER]

Thanks,

I'm always encouraged by Canyon's posts, although i have become numb to ESPR buyout optimism.

[Gregg4]

I agree let's get moving. Just posted on Stocktwits.

[FACT-MASTER]

Amgen released 4th quarter details today with a significant increase in sales of Repatha:


https://www.reuters.com/business/healthcare-pharmaceuticals/amgen-profit-beats-estimates-next-maritide-studies-start-by-mid-year-2025-02-04/

"The company's fourth-quarter sales of Prolia, also known as denosumab, rose 5% to $1.2 billion. Sales of cholesterol-lowering medication Repatha rose 45% to $606 million, while sales of arthritis drug Enbrel were flat at $1 billion."


Amgen's numbers are impressive imo. ESPR mgmt. is wasting valuable time in getting their marketing strategy going,,,,well, i guess that could be a matter of perspective, eg: sk may be thinking "nascar" is great,, however, imo, nothing is working for ESPR, and sk doesn't care.

[Gregg4]

I agree and it's time better spent at where when our money comes from anyways, right

[FACT-MASTER]

Not sure, decided to stop watching and focus on my work related projects and goals - much more satisfying.

Haven't sold any ESPR, and am the type that will go down with the ship ( if necessary, but hope not).

I only skim through the st board now, however i like the idea with Cramer video, and analysts putting forth more blunt questioning at ESPR's quarterly calls. ( think that was Canyon)

I was reading one post by Gary where he elaborated on buying in the 20's and then averaging down to the 2's. I wonder if this is / was the case with institutions as well, and thus a possible reason for the huge issuance of shares, especially in 2024 - to assist institutions in lowering their average cost base on their ESPR share holdings.

As is the case more often then i like, time will tell here.

[Gregg4]

You think we will get anything from DSE tonight?

[Gregg4]

Great information thanks

[FACT-MASTER]

and yet more on ACLY inhibition going on at Espervita in the area of liver cancer https://www.espervita.com/science.php ( Gregory Steinberg, PhD - founder), former Esperion founder Roger Newton. https://www.espervita.com/about.php and 2 more Esperion founders, keep reading the last weblink, i'm going to get timed out here in a second.



This Canadian connection is mind boggling, however the dots are connecting now with the OMERS deal, and the convertible financing and everything Canadian.

Now if we can just get that connection with Denmark ( Novo Nordisk) , the story could get very interesting here with ESPR. Being a European based company NVO would know first hand about the uptick in European BA sales going on at DSE.

https://companiesmarketcap.com/cad/novo-nordisk/marketcap/

omg here comes our waitress, gotta run.