Member Info for sadoldgit

Not a lover of AI.

Came across the folliwing a while ago.

Yes, Contract Research Organizations (CROs) that carry out toxicology testing on animals are required to check the suitability and safety of the excipients used in their study formulations.Excipients are not simply inert carriers; they can introduce hidden toxicities or interfere with the study's scientific validity.

Good morning HbD

All Tyk2 inhibitors are not the same. Takeda is of later generation.

'Target Selectivity: While all allosteric inhibitors are highly selective, they differ by orders of magnitude. For example, the FDA-approved deucravacitinib has roughly an 87-fold binding selectivity over traditional JAK enzymes, while next-generation candidates like zasocitinib (TAK-279) demonstrate over a million-fold greater binding selectivity.'

Yes both still have mono inhibition by Tyk2.

Greater efficacy can be achieved by dual inhibition but again selectivity and molecule size are crucial in some indications. BBB and CNS being one.

Regards

Ai response npt the be sll.amd rnd all.of vourse but an indication of approximate timelines.

'Producing a comprehensive toxicology study report post the 16-week (90-day) in-life phase typically takes 8 to 12 weeks. The entire process—including bioanalysis, histopathology, peer review, and final quality assurance (QA) sign-off—results in an overall reporting time of roughly 3 to 4 months after the final animal is necropsied.

The timeline is driven by several key post-study data evaluation stages:Bioanalytical Analysis (Weeks 1–4): Processing and analyzing blood, plasma, and tissue samples to determine drug exposure levels (pharmacokinetics).Histopathology & Pathology (Weeks 2–8): Evaluating tissue slides and organs. This is often the most time-consuming step due to the thorough microscopic examination required for long-term studies.Drafting the Report (Weeks 8–10): Toxicologists integrate clinical observations, clinical pathology, and histopathology data to draft the comprehensive study report.

QA Review & Finalization (Weeks 10–12): The draft undergoes intense quality assurance auditing, sponsor review, and final pathologist/study director sign-off to ensure regulatory compliance.'

Difficult to release data from an uncompleted report without causing problematic intepretations on the data released.

Some data will.be known already as in establishing an MTD.

Nice to know and conforms to legislstive requiements but we are looking at long suitability for long term use.

Font just look at what w801 can potentially do but also gor how long for ie a lifetime in cerain indicstions like plaque Psoriasis.

Any interested party sits in the same boat as us. They will want to know safety and efficacy and most certainly suitability for longterm use.

Just how big can an inhibitor capture of a wotlwide market with a commercialised 1801 initially focusing on Psoriasis?

1803?

Nobody knows as early stages with investigstions showing possible potential in BBB and CNS.

Definately need an update on this even if only to say still.progressing.

Regards

Ai response npt the be sll.amd rnd all.of vourse but an indication of approximate timelines.

'Producing a comprehensive toxicology study report post the 16-week (90-day) in-life phase typically takes 8 to 12 weeks. The entire process—including bioanalysis, histopathology, peer review, and final quality assurance (QA) sign-off—results in an overall reporting time of roughly 3 to 4 months after the final animal is necropsied.

The timeline is driven by several key post-study data evaluation stages:Bioanalytical Analysis (Weeks 1–4): Processing and analyzing blood, plasma, and tissue samples to determine drug exposure levels (pharmacokinetics).Histopathology & Pathology (Weeks 2–8): Evaluating tissue slides and organs. This is often the most time-consuming step due to the thorough microscopic examination required for long-term studies.Drafting the Report (Weeks 8–10): Toxicologists integrate clinical observations, clinical pathology, and histopathology data to draft the comprehensive study report.

QA Review & Finalization (Weeks 10–12): The draft undergoes intense quality assurance auditing, sponsor review, and final pathologist/study director sign-off to ensure regulatory compliance.'

Difficult to release data from an uncompleted report without causing problematic intepretations on the data released.

Some data will.be known already as in establishing an MTD.

Nice to know and conforms to legislstive requiements but we are looking at long suitability for long term use.

Font just look at what w801 can potentially do but also gor how long for ie a lifetime in cerain indicstions like plaque Psoriasis.

Any interested party sits in the same boat as us. They will want to know safety and efficacy and most certainly suitability for longterm use.

Just how big can an inhibitor capture of a wotlwide market with a commercialised 1801 initially focusing on Psoriasis?

1803?

Nobody knows as early stages with investigstions showing possible potential in BBB and CNS.

Definately need an update on this even if only to say still.progressing.

Regards

Hood morning Mayhem55.

My sentiments exactly.

Turning point July 24 when TM stepped down as CEO.

I dont believe it was coincidental that TM took up development of a new compound shortly after strpping down.

It is unlikely that being involved with the day to day stresses as a CEO in current financial climate would enable Tim to focus on the all important development.

Should see news on two fronts from 1801 and 1803?

Phenomenal potential commercialisation value should 1801 prove top notch and significant positive progress on BBB and CNS indcations.

Yet at the present time we sit at a paltry 30 odd million market cap. Nothing is 100% guaranteed reflected in current SP!

One thing for sure is that should an attempt have been made to establish an MTD that that result will already be known.

I am 100% certain this would have bern performed as is part of the new post 21 regulatory requirements that were fully entered onto government website early 2024.

We are exploring the probabilities of 1801 for longterm treatment in indications, possibly life long. Condiderable value here.

Regards

Good morning DP64 l rust you are well.

An article from the thoughtful WSJ in the link that may or may not interest you depending on your agenda.

https://www.wsj.com/health/pharma/big-pharma-is-thinking-small-on-deals-thats-a-boon-for-biotech-43577087

Regards and time for a beer or two.

Good morning everyone.

Much discussion about the toxicology study.

Whilst the shareholder is keen to be kept informed of developments it is also vitally important for Sareum and any potential buyer/partner.

Some info below.

Sareum as far as l know have not expressed any urgency in raising funds. Unusual as indeed Potnak pointed out.

The timeframe from a pharma company’s initial outreach to an official deal offer (term sheet) to a small biotech typically spans 2 to 9 months, with some clinical-stage deals taking up to 1–2 years.

The process is driven by data reviews, stakeholder alignment, and the asset's clinical stage.The timeline breaks down into four core phases:

1. Initial Engagement & Confidentiality (2–4 Weeks)First Contact: The process begins with an introductory pitch at an industry conference or direct outreach from a pharma Business Development (BD) executive.CDA and Data Room: Once mutual interest is established, both parties execute a Confidential Disclosure Agreement (CDA). The biotech provides a non-confidential pitch deck, followed by deeper, confidential data.

2. Scientific & Strategic Triage (1–3 Months)Internal Triage: Pharma BD teams triage hundreds of opportunities yearly. They present the science to internal R&D and commercial committees to secure an "internal champion".Meetings: Expect multiple deep-dive scientific and operational discussions to align on development, regulatory strategy, and manufacturing readiness.

3. Due Diligence (1–4 Months)Data Room Opening: The pharma partner activates a broader team (legal, financial, regulatory, IP, clinical) to rigorously audit the biotech’s data room.Dilution & Validation: This stage tests the robustness of your preclinical models or clinical efficacy. The pharma may request confirmatory studies or additional documentation.

4. Term Sheet Negotiation (2–6 Weeks)The Deal Offer: If due diligence is successful, the pharma BD team will submit a formal term sheet outlining the deal structure (e.g., upfront payment, downstream development/commercial milestones, and royalty tiers).Finalizing Terms: Although a term sheet takes only a few weeks to finalize, complex negotiations can extend this if the biotech's cash runway is short and the pharma partner attempts to shift most of the value to downstream milestones.If you are currently evaluating a partnership, let me know:What clinical stage is your lead asset (preclinical, Phase 1, Phase 2)?What therapeutic area does your technology address?Roughly how many months of cash runway does your biotech have?I can provide negotiation benchmarks or evaluation criteria specific to your situation.

AI l know but could be fun as well as eye opening to delve.

Patience.

Regards to all

good data given. jak2 ****dimerisation clearly no problem at these doses. slight adverse event with one patient that had history of high glucose and proven to be type 1 diabetic.

all very good.

link below should give acces to requirements and procedures in toxicology testing.

pertinent areas here in safety so may l be so bold to suggest a mtd will be established.

it is not so much as jr stated that pharma preferred a maximum tolerated dose but a requirement in section s3.

https://www.gov.uk/guidance/international-council-for-harmonisation-of-technical-requirements-for-pharmaceuticals-for-human-use-guidelines

question of course here is where does 1802 fit in?

1802 is badged as a possilbe back up for 1801 and is this is reinforced by patent protection and description of patent related to.

due to the slight difference in selectivity of 1801 and 1802 it is not beyond belief that it may well be in the planning at later stage that incombo therapy of 1801 and 1802 woild provide greater efficacy over cd and uc as in many cases bowel cancer follows at a later stage.

all quiet on the bbb cns front as with 1802.

a positive development on both fronts here will most likely lead to a buyout. that is my opinion.

regards and good day to all

The extra time taken to reach nigh perfection will be worthy if the result is my guess.

Plenty of other inhibitors out there.

We will better deucravacitinib in efficacy and far supetior safety profile to Breprocitinib.

Yes these chappies have generated compounds but pretty certain will readily be bettered by SDC1801. That is based on what l believe l know.

There are some that will disagree.

The likes of PC1954 and the insulting MK Don to name but two.

No real concrete factual evidence provided by either in any dispute or disagreement.

Not worth a bladder full of cold pee as far as l am concerned but give them both credit for the resurrection of a fund raise a couple of years back along with Billy Bunter.

Regards and a good day to all whatever your agenda

Ai is not the be all and end all.

No such thing as the toxicology study being a failue per seh.

1801 has already established a far superior safety profile to Breprocitinib our most competitive competitor.

Suitability for longer term treatments of 6 months or more to possible life long treatment is the purpose of the study as well as a Ststutory requirement since Brexit albeit legislstion not updated until around 2022 to include now mandatory long term toxicology testing.

A very likely cause if the MHRA debacle l would hasten to add.

The safety of Tyk2 inhibitors has been endirsed by the likes of Deucravacitinib. Deucravacitinib, l wonder how they created that name?

May I suggest that is due to the use of a Deuterium Hydrogen element that enables greater binding affinity by the addition of the mass of the neutron effectively doubling its mass. Although having no charge it does change the behaviour as the mass of the nucleus is increased.

A Deuterium bond vibrates at a lower frequency due to the greater mass of the nucleus.

It has a lower zero point energy and hence requires more energy to break the bond.

Now the use of Jak inhibitors has a history of unwanted off target effects.

No such thing at the moment is a pure Jak1,Jak2 ir Jak3 inhibitor.

What exists is selectivity over. Early generation not nearly selective enough hence poor performance in efficacy/safety profile. Dose limiting toxicity!

We are l believe around 90 to 95% selective of Tyk2 over Jak1

Our Jak1 is around 4 to 5 fold selective over Jak2 and Jak3.

No Jak2 inhibition observed in phased SAD and MAD study. By this it means biomarkers leading to off target adverse blood plasma events caused by h0modimerisation of Jak2.

For whatever reason this is not happening here. It may well be heterodimerisation of jak1 and Jak2 or Jak2 and Tyk 2 both of which would prove beneficial as no unwanted off target adverse events as a result.

It is not unreasonable to suggest that the 'optimal amount of Jak1' present in 1801, not only enhances the efficacy of Tyk2 but also with no detectable Jak2 activity in SAD and MAD phase1a studies, maintains a nigh if not identical safety profile.

Dual inhibition efficacy whilst maintaining allosteric Tyk2 safety profile.

AI that f...er!

Please have the decency to allow several days after dosing has completed as study does not end on last day of dosing.

Patience is a virtue.

All will be revealed soon.

It is not just the investor here that has its eye on the compound but also interested pharmaceutical.

Take the buyout of SO by GSK.

Regards to all the genuine.

Good afternoon PC1954.

Not wishing to pull your post apart, but

'There is a misconception on here, if people think that week 16 is the “tick box” for SDC-1801, it’s only the dosing period - data analysis, evaluation and reporting of GLP on all matters relating to that dosing to be scrutinised before regulatory submission to MHRA for efficacy to continue into Phase2 trials.

'regulatory submission to MHRA for efficacy to continue into Phase2 trials.'

Toxicology pertains to the safety with respect for suitability for long term use, it has absolutely nothing to do with efficacy apart from establish if any dose limiting toxocities.

Indeed there are many indications.

With regards to a 16 week trial there will be preliminary results just as there were in phase 1a trial.

This is the teaser of course. As the maximum dosing reached will be known and also adverse effects if any. ( 1802 will be a tad different of course)

However, it also needs to be taken into consideration that dosing of animals in mg per kilo weight differs significantly in dosing human mg per kilo as metabolism is vastly different unless of course using primates.

As l am sure you understand around two thirds of compounds fail in a phase 2 study. This is in the main due to Dose Limiting Toxicities.

A drug can pass in a phase 3 clinical study but at a later date fail at a later phase 2 in a different indication. As an example Deucravacitinib authorised for use in Plaque Psiriasis but failed dismally in Ulcerative Colitus.

With regards to efficacy in a psrticular indication this is determined by phase 2 trial.

Let me remind you of the interview involving John Reader with the identified target of Il-6 Il-17 Il-22 Il-23 interleukins as well as interferon gamma crucial in many indications.

In effect it is the inhibition of these targets that will lead to satisfactory efficacy. Unwanted inhibition of targets outside these areas or unbalanced inhibition highly likely to give rise to unwanted off target events that will compromise efficacy v safety.

As both JR and TM have stated we will be better in some indications and not so good in others ie Sotyktu, as we are a dual inhibitor of Tyk2 with what TM described as their belief of the optimum.amount of Jak 1 hence best of both world in a compound.

Full confurmational results are still undeniably crucial.

My opinion FWIIW is outright buyout or as back up an onlicence or partnership on more than ome front.

All of our compounds are available and no complications as such if total buyout is the objective. Known as optioneering.

These are what l believe are Sareums objectives but outcome is anyones guess.

Regards

Good afternoon PC1954.

Not wishing to pull your post apart, but

'There is a misconception on here, if people think that week 16 is the “tick box” for SDC-1801, it’s only the dosing period - data analysis, evaluation and reporting of GLP on all matters relating to that dosing to be scrutinised before regulatory submission to MHRA for efficacy to continue into Phase2 trials.

'regulatory submission to MHRA for efficacy to continue into Phase2 trials.'

Toxicology pertains to the safety with respect for suitability for long term use, it has absolutely nothing to do with efficacy apart from establish if any dose limiting toxocities.

Indeed there are many indications.

With regards to a 16 week trial there will be preliminary results just as there were in phase 1a trial.

This is the teaser of course. As the maximum dosing reached will be known and also adverse effects if any. ( 1802 will be a tad different of course)

However, it also needs to be taken into consideration that dosing of animals in mg per kilo weight differs significantly in dosing human mg per kilo as metabolism is vastly different unless of course using primates.

As l am sure you understand around two thirds of compounds fail in a phase 2 study. This is in the main due to Dose Limiting Toxicities.

A drug can pass in a phase 3 clinical study but at a later date fail at a later phase 2 in a different indication. As an example Deucravacitinib authorised for use in Plaque Psiriasis but failed dismally in Ulcerative Colitus.

With regards to efficacy in a psrticular indication this is determined by phase 2 trial.

Let me remind you of the interview involving John Reader with the identified target of Il-6 Il-17 Il-22 Il-23 interleukins as well as interferon gamma crucial in many indications.

In effect it is the inhibition of these targets that will lead to satisfactory efficacy. Unwanted inhibition of targets outside these areas or unbalanced inhibition highly likely to give rise to unwanted off target events that will compromise efficacy v safety.

As both JR and TM have stated we will be better in some indications and not so good in others ie Sotyktu, as we are a dual inhibitor of Tyk2 with what TM described as their belief of the optimum.amount of Jak 1 hence best of both world in a compound.

Full confurmational results are still undeniably crucial.

My opinion FWIIW is outright buyout or as back up an onlicence or partnership on more than ome front.

All of our compounds are available and no complications as such if total buyout is the objective. Known as optioneering.

These are what l believe are Sareums objectives but outcome is anyones guess.

Regards

An easy by longish read below. From 2025.

https://www.explorationpub.com/Journals/eds/Article/1008116

Good morning PC1954.

Two posts were made. Presenting a post is not an attempt.

You were asked from whence and where did l give you cr.p as you claimed.

Clearly l did not. But you lack the integrity to at least acknowledge.

Provacative?

I suggest you have a look through some of your posts.

If in doubt l can copy and paste.

Regarding reality?

Are you implying that potential is not part of reality?

If the potential is reached it becomes a long awaited achievement that will ultmately be reflected in the market cap. However, without potentual we would indeed be subject to further decline.

I note no comnent with regards to importance of IL-22. Clearly you cannot comprehend that which l post so may l suggest you use AI?

AI is not infallible and does frewuently get things wrong or make false assumptions leading to incorrect information.

Good that you are having bowel screening presumably on a regular basis. Early diagnosis leads to early treatment and potentially proper control or cure.

As l am sure you are aware processed foods are one of the major causes associated with bowel cancer. To a certain degree also red meat.

Of importance is a balanced diet of course. Has a marked effect on our immune system.

However, in an age where convenience foods have become the norm it is no suprise that we are a nation suffering with obesity and bowel complications.

Regards to me being a Hammer and your 'dissapointment on my provacative stance' i tend to focus on what we can achieve as opposed to where we stagnate at the moment.

Early part of life l worked in mechanical engineering with time spent in research and development. The dreaded 725 Die Platten Cutter.

Revolutionary but sinple in design with the intention of achieving far greater output by utilising 4 crankshafts instead of two camshafts.

It was a US company thst went bust fue to debts in Harlem and Dundalk, Leiston was profitable .

Enjoy your day

I must apologise for my apalling spelling mistakes PCS1954.

I should correct my spelling mistakes prior to submitting the post.

I am restricted to this little mobile phone with tiny little keys and oh so easy to hit wrong key.

Do you think that it may be a possibility that Laboratory testing periodically of patients may be reduced or required less frequently dependent on toxicology results?

FWIIW my opinion is that the level of Laboratory testing will become apparent in the first clinical trial in Plaque Psoriasis. Requiring in the end perhaps a 12 month or routine blood test and count.

Of course the same conditions would not apply to 1802 due to the higher Jak content, unless used in autoimmune as originally intended for immuno oncology.

As for values, is it not nigh impossible to assign a value to Sareums entire compound range both individually and collectively? Imperative that indications suitable for commercialisation are identified via high efficacy and satisfactory safety profile?

It is my belief that there are ball park figures subject to results, all in discussions and of course informal, the critical component being 1801 closely followed in advances in blood brain barrier penetration for diseases pertaining to the central nervous system.

Potential here of course, as Interleuken 22 identified as major contributory factor in both MS and AZ.

Sareum 1801 already proven preclinically to inhibit IL-22, However, crossing BBB and the behaviour of kinase inhibitor compounds in cerebral fluid is vastly different to plasma.

I still remain optimistic on more than one front.

Nighty night

Ps l am pretty certain there is only one spelling mistake.

PCS1954,

You really are a one aren't you

You were asked exactly as to how exacyly have l given you Cr.p?

I have not. That is the answer.

An over reactuin by you at a quarter ti 12 at night.

A few too many or aee you Chalfonts playing yiu up old son.

You post regarding respected posters.

You have shiwn very little respect.

You clearly are unable to hold dialogue regarding the science. Tell me is this down to ignorance or the inability to comprehend basic chemistry and biology?

I put questions too you regarding our and competitors conpounds. Clearly the above paragraph applies to you here as relavent here as confirmed by your dissapearance to Italy and remark about not looking at the 'bb'

You post AI data. No difference to that l was saying 18 months ago.

Long term toxicology study to enable phase 2 studies with high degree of success as will prove suitability for long term use periodic or otherwise as will not suffer from the restraints of dose limiting toxicity.

The question is as follows.

On favourable toxicology results, does SDC1801 a Tyk2 Jak1 inhibitor come under the classification of a Jak inhibitor requiring constant periodic laboratory testing in clinical trials that allosteric Tyk2 appears to be exempt from?

These labaratory tests as l am sure even you are aware are very costly.

Nighty night

Good evening PC1954.

Thankyou for your reply but you did not address the points l made.

1. Is Breprocitinb more advanced than Sareum?

It is more advanced but certainly does not make it worth more.

It is all down to safety and efficacy.

2.Dual inhibitors preclinically proven to have greater efficacy than Tyk2 alone.

3. However, Jak inhibitors as such relates to the early generation, were poorly selective intentionally to give broader scope or not.

This lack of selectivity gave rise to serious adverse events including Major adverse cardiac events.

4. It is not beyond the realms of belief that just maybe we have the best of both worlds here.'

5 We are also encouraged by the continuing TYk2 with no safety concerns. Sareum themselves stated this as l am sure you are aware.

With a good toxicity profile we will not be hampered by dose limiting toxicities with the resultant more than satisfactory efficacy result in numerous indications. The more approved indications the greater value.'

I bought Thoths figure in of 14 pounds a share as derived from 1 billion market cap with 70 million shares in issue.

A poster here put a value on Sareum of 2 billion recently.

The point l were making is that with 140 million shares in issue would make each share 14 pounds each.

So in essence, not predicting £ 14 a share merely that it is a possibility.

Huge advances would need to be made on all fronts.

In my opinion for what it is worth is that dear old Sareum will be taken over providing ;-

1.SDC1801 completion toxicology study allowing authorisation for long term use.

2 The possibility of treating CNS indications i given in preclinical testing.

Funding at some stage will be required if we are not bought out.

I am not taking this personal as indeed it were a short while ago deliberately set out to undermine.

You want to play little games PC1954 then do so. I thought you were beyond that. I have never given you any crap. I am more than capable of doing so.

Night night

Good morning PC1954,

Is Breprocitinb more advanced than Sareum?

It is more advanced but certainly does not make it worth more.

It is all down to safety and efficacy.

Dual inhibitors preclinically proven to have greater efficacy than Tyk2 alone.

However, Jak inhibitors and thus relates to the early generation were poorly selective intentionally to give broader scope ir not.

This lack of selectivity gave rise to serious adverse events including Major adverse cardiac events.

It is not beyond the realms of belief that just maybe we have the best of both worlds here.

Long term toxicolgy results will give suitability for long term use.

We are also encouraged by the continuing TYk2 with no safety concerns. Sareum themselves stated this as l am sure you are aware.

With a good toxicity profile we will not be hampered by dose limiting toxicities with the resultant more than satisfactory efficacy result in numerous indications. The more approved indications the greater value.

Nothing 100% guaranteed of course.

I am not sure why you think my posts are hyoerbole as what is written above is basically fact.

Are you of the opinion that Thoth2 posts were 'hyperbole' regarding £14 a share, ie around 1 billion. Interesting l note that you are looking at a figure of 0.9 billion in one of you recent posts.

From where do you derive this figure? Is this not hyperbole too?

There are twice the amount of shares now and we are further forward with 1801 1802 and now looking in to diseases of the central nervous system with a compound we have has being identified as showing potential but requiring optimisation.

Yes we do still have hurdles. We have increasing competiveness and more biotechs entering this arena and vast strides being made in China

In my opinion the current SP in no way reflects the value of what we have.

What is does reflect is the value of Sareum market sentiment.

Investors moved out out of biotech after the covid peak and rapidly invested into the military manufacturing companies.. to invest in guaranteed returns in this indusry eg Rolls Royce up 1200 percent in 5 years investors will not be looking into high risk albeit potential high gains, hence phenomenal market Cap decreases in small bio with many going under.

The question here of course is as follows.

Is a world class inhibitor worth more or less to a buyer than say 6 years ago?

If the market Cap of a company drops 90% does the value of its pipeline drop by 90%?

Mayket sentiment is a strange beast.

Regards to all

Where exactly us the insubstantiated hyperbole.

The price of a biotech company is valued on its pipeline not tge size of the company.

Momoletonib was owned by Sierra. 1.9 billion was paid by GSK.

Momoletonib has nowhere near the potential market as the likes of Sotyktu or indeed TAK-279.

Once a compound has approval in an inducation it will be snapped up by big pharma. Then it is commercialised by trialling it in every indication they can.

GSK Momoletonib is one example but of course limited in indicstions.

Chk1 and Wee 1 inhibitor returned to sender.

2 billion l would personally put on a value with great results on tox trial and approval for Plaque Psoriasis.

BBB achieing any sign of potential should significantly increase the SP

Agree with Potnak looking at sround 2 years perhaps a tad less. Certainly l would not value Sar at 2 billion at the moment. Possibly worth as much as 400 million on decent tox results.

Efficacy should not be a problem in Sareums stated indications as highly unlikely 1801 would suffer dose limiying toxicities experience wuth othe Dual inhibitors including our most advanced competitor Breprocitinib.

Where is the insubstantiated hyperbole in this?

Biopharma market suffered as all investment now mainlt to do with military sector. Many with a thousand per cent increase over past 5 years.

Regards

Good afternoon Steve i am of the same opinion myself eith regards to selling the company.

TMdis mention 2024 AGM that they were all getting on and if an offer was placed which they deemed reflected the value they would accept

1801 has not really progressed since July 24 with exception of now recomnence ment of trial.

It does bug me that a CRO that is regulated and has a duty of care to animals allowed a compound with a non safe excipient to be used. It is normal procedure for a CRO to go down that route.

A new batch of 1801 had been made up and deluvered to CRO. Question here is had the excipient ie the carrier already been included in the compound?

Blood brain barrier penetration and CNS indications?

It would not be unreasonable to expect progress development in next few weeks.

This in effect is an untapped market with huge potential for any inhibitor that has a positive result with respect to a treatment that even just limits progression. MS similar to SLE except MS is CNS and SLE is PNS ( peripheral nervous system).

Should 1801 and BBB CNS compound materialise then Thoths 14 pound a share becomes a possibility. A 2 billion buyout with 140 million shares balances nicely.

That of course not inclusive of 737 and 1802.

One thing however is that, how much value a compound has is not always reflected when offers are made. Pharmaceuticals are a business and a very cut throat one at that.

When positive news does come through expect a significant rerate!

Ideally the efficacy of Jak inhibitors with a safety profile of an allosteric Tyk2 inhubitor is the objective. This would be a first.

Regards to all LTH