Member Info for sadoldgit

Goodevening HbD.

As far as l know phasex3 could continue with 737 and LDG or Cisplatin

A phase 2 trial l believe could follow multi in combo therapy.

Very little point in applying to healthy humans as criteria a tad different in oncology

For example you are not going to administer chemo to a healthy person.

The majority of volunteers that we had, had previously gone through many other forms of treatment thst the cancers had developed resistance to.

Good results in Phase 2 possibly following a phase 2a to establish proof of concept would allow entry to phase 3.

Phase 3 costly with many hundreds of patients.

A 7am RNS would be very nice indeed.

Regards

Goodmorning Celtic007.

I'm OK ty.

With regards to 737 and the onlicence , in my opinion it is either an associate or ex associate connected with SO, or a chinese pharma.

The long period of 8 months suggests to me that is a chinese pharma development company in the US.

There was no news when development of the issues of solubility on Aurora FLT3.

It was returned following no success in this area.

Not the same as an on licence it has to be said.

The only way forward for CHK1 inhibitors exist in combination therapy.

That applies to all of this type of inhibitor.

In effect it Chk1 limits the growth of cancer at the point of cell mitosis.

It does nothing to kill the current cancer as such.

Hence chemo causes death to cancer cells and also creates damage to cells.

Chk1 can then prevent these cells multiplying via DNA damage repair cycle.

Monoclonal antibodies can also attack cancer cells causing cell death.

If we combine chk1, monoclonal antibodies that recognise the cancer and destroy plus chemotherapy very satisfactory results can potentially be achieved.

The only niggle with being a chinese pharma is the on licence is very little difference to the original licence made with Sierra Oncology.

737 should be at minimum phase 3 combination trials by now to meet areas of continuing unmet need.

Regards

Good morning HBD.

I had posted before of Chinese companies in the US that progress drug development. There are many.

If we take an excerpt from 2nd Jan RNS you will see it states based in the US.

SRA737

Cambridge, UK, 2 Jan 2024 - Sareum Holdings plc (AIM: SAR), a clinical-stage biotechnology company developing next-generation kinase inhibitors for autoimmune disease and cancer, today announces that the Company's co-development partner, the CRT Pioneer Fund ("CPF"), has entered into a development and commercialisation licence agreement for SRA737 (the "Licensing Agreement") with a private biopharma company based in the United States (the "Licensee Company").'

It does not state that it is a US privately owned company.

Regards

A link below regarding Psoriasis.

This is not the company claim about Ropsacitinib, but a list of inhibitors which grow all the time.

Worth a glance through as is a very long read.

https://www.mdpi.com/1999-4923/16/2/239

Regards.

Good morning HbD.

There also exists Ropsacitinib which is a Tyk2 Jak2 inhibitor which so far is claimed not to have any Jak2 adverse effects. That is what l see is our biggest threat should the claim work out as claimed.

Problems with Jak2 with ho,modimerisation leading to severs adverse effects.

Regards

Damion,

'no guarantees for 1801 in psoriasis even the bod have no idea how it will perform they only chose psoriasis as it was the easiest to recruit and the cheapest way forward.'

Misinformation you have posted.

Tim stated in interview with Andrew Scott that we as in Sareum believe we can provide greater efficacy than Deucravacitinib in Psoriasis as is dual inhibition.

Clearly you are not aware of this information.

Fannyguy posting early pre open negatively as pee normal.

Reality 10 l have given a figure now answer the question that l put to you.

You really are making statements giving absolute confirmation of the ill educated, ignorant cess pit that you are.

Are you tied to that Puma via an umbilical cord?

No idea myself and you are that devious I would not trust your answer anyway

Regards and don't forget to get up first thing and post your or so unsubstantiated negative bs

It's ok, l am not feeding trolls, feeding monkeys.

Clearly the monkey is brighter and has the ability to reason.

Based on late stage Deucravacitinib at 4 billion and take a 99% chance we outperform Deucravacitinib then a deal worth 500 million to 1 billion plus inclusive of milestones is most likely.

Tell my sonny boy what is wrong with this reasoning.

Tell me in your very simple mind why 1801 should not out perform Deucravacitinib in psoriasis?

Tell me who is our biggest threat in Psoriasis and the reason for.

You started this debate, prepare to get eaten alive

All comes down to the in depth safety data and if all bodes well I will not be far out.

Reality 10.

As I have said figure is dependant on the development news and that relies to the full data results in detail supplied to an interested party.

Really sonny you are way way out of your depth.

Really on your ignorance you are asking nothing more than how long is a piece of string.

You need to grow up.

Reality10

I will ask you a question.

Deucravacitinib was sold for 4 billion dollars.

The be be all and end all of a safe inhibitor that 'regulates' the active site through the allosteric pseudo domain.

This is stated by BMS

Is this information doctored as in a salesmanship like claim as opposed to actual scientific all researched papers and if not why did it fail to meet it endpoints in phase2 Ulcerative Colitus?

The placebo was indicated as more effective!

Tell me why or even perhaps have an attempt at it.

Prepare to get eaten alive here on a debate

Regards

Reality 10 you soppy little boy.

The news is not what is contained within the data.

The news will be as in how further development is progressed

The full data given to interested parties are way above the level of understanding here by most.

That to certain extent includes myself.

For example educate me in the Indications that 1801 is likely to prove most successful in.

From what and how is this information obtained and the relevance thereof.

What are the negatives and positives from phase 1a data that indicate very likely success?

Take as an example IL-10.

Does Tyk2 inhibit IL-10?

If it does tell me why it does. I will tell you why it will not not.

What is the significance?

I have posted many times on this before, some people will read and some will not as can't be bothered to read.

Not my fault people don't understand.

Some people try to and l like to explain if asked.

I suggest you spend a little more on understanding what we have.

Your agenda is clearly see through.

Share is going to drop, at the same time on news rise your opinion is 50 to 70p.

Why not hold in case news comes faster than you think?

What data are we talking about?

Safety data?

What we have so far enables us to progress to phase 2 trial.

Is that right or wrong?

Correct me if l am wrong.

Put a price on an upfront on licence on 1801 if you have that ability.

If you cannot then your reasonings are somewhat futile as have no idea.

Tell me what the advantages are over a dual inhibition inhibitor over allosteric Tyk2.

Tell me what the downsides are?

I am here to on licence and or take over fact.

You entered on LSE 23rd Aug 23.

Similar to times entered by

MAJWandCo

Puma

Robinhoodof AIM.

You are no different and in more ways than one may be the same.

Clearly you not have any understanding as to what is our pipeline.

The price until a deal of somesort materialises, will go up and down.

Reality 10 your expectations are nothing more than an opinion?

On what factual basis do you make such statements?

Deucravacitinib was 4 billion at end of stage 2 trials.

Indications as such very strongly suggest we will have greater efficacy in Psoriasis alone with similar safety profile.

The reasonings and logic behind this, l understand. Clearly you cannot comprehend?

Nothing factual apart from your expectation.

You pays your money you take a chance.

I expect multitudes of current SP as what we currently own?

Tell me what is wrong with my expectation and the reasonings behind it

Https://finance.yahoo.com/news/bristol-myers-sends-tigit-drug-112300056.html

Question here is what do they have to replace it with

Damion, Agree wholeheartedly.

What relevance is it to us to know the fine detail?

What would be the point of releasing an RNS unless progression in whatever format is also released?

Negotiations of somesort will be in place.

If more than one party thst gives options.

Tim l don't think cut out for this, scientists are not good salesman.

Hence he is now COO to concentrate on pipeline.

Onlicence very likely in my honest opinion or a non dilutive arrangement of somesort.

Ideally it would be fund phase 2a trial and take from there?

How many other Indications are we likely to be as good as if not better than competitors?

Do they want 1801 on its own or inclusion of 1802 subject to final phase trial in oncology indicatuon?

Very likely we have received the data, but any interested party will also need evaluate the data.

In addition the data will need to be utilised to enable safety case for progression to phase 2.

What we lnow so far is that subject to funding we can enter phase2 in any indication deemed to be commercially viable.

Regards

Regards

A excellent post Potnak which l recommend highly.

Very rarely l pay you a compliment.

Regards

'Anyone who wanted 120 could have sold this time last year but didn't. This isn't the right time for bids & offers, let them get on with the job in hand.'

It is not a case of what anyone wanted 120 last year could have sold.

I have merely put the together the 800 million a piece which Tim valued over a couple of years ago. 10 to 1 risk factor.

This is an absolute minimum as l would see it.

Pharmas are not your friends, they did not get to where they are by being nice.

Anyone wanting 120p could have sold last year whilst true doue not take into account anyone who bought this year at 10 12 15 or 20p wanting to sell at 60p ie half 120p

The market Cap circa 30 million at the moment which is way way below the value of the compounds we have at this stage.

Companies can make informal offers as they see f fit.

It looks to me as you have completely misinterpreted the intent of my post. Perhaps l should have detailed further for which l apologise.

Regards

cct245737 (21, sra737) is a clinical candidate for chk1i, originally derived from the purine template hit 18.

the initial optimization aimed to improve the kinase affinity and selectivity by targeting the interior pocket of chk1, generating compound 19. the pyrimidoazaindole tricyclic scaffold was designed with a pyridine moiety located into the specificity region and an additional nitrogen atom contacting a water molecule. however, compound 19 exhibited issues with conformational deviation and molecular rigidity

[70]

. through further optimization, the five-member ring-disconnected compound 20 (cct244747) was obtained, which maintained the high intrinsic potency, selectivity and cellular activity. besides, cct244747 has been identified as an orally effective single agent in a mycn-overexpressed neuroblastoma model

[71]

. however, cct244747 had low metabolic stability in human hepatocytes, and with oral bioavailability of only 61 %), high doses were required. subsequent work focused on the 4-position of the pyridine substituents situated in the ribose binding pocket of chk1, which was confirmed to maximize affinity. a diverse set of 4-amino-substituted pyridine derivatives were synthesized, unexpectedly, resulting in the clinical compound cct245737, which exhibited the excellent chk1 enzymatic activity (ic50 = 1.3 nm), increasing metabolic stability, and improved pk properties with reduced in vivo clearance and good oral bioavailability of 100 %

[72]

. fan et al. confirmed a strong synergistic anti-cancer effect of cct245737 and vp-16 in chronic myeloid leukemia (cml) cell line k562. furthermore, cct245737 prevented vp-16-induced g2/m arrest, inhibited both brca1 and rad51 (the most significant component of the ****logous repair pathway) and induced cml cells apoptosis

[73]

. the result of the phase i/ii clinical trial (nct02797964) showed that cct245737 was well tolerated and had good pharmacokinetic profiles (t1/2 = 6.23–10.4 h, cl/f = 18.4–119 l/h, vd/f = 215–1590 l). however, the single-agent potency of cct245737 was not considered to be significant enough for development as a monotherapy for cancer. therefore, subsequent clinical trials will be conducted in combination with other drugs

Good morning The Oracle.

Personally l don't see the Sareum Kinase inhibitor library is the elephant in the room per seh.

The 30 or so molecules which are patented hold the true elephant in the room and of course this detailed information will exist in SKIL.

As an apology take two towns connected by one straight road. That is the simplist way and most effective of getting from A to B. Take the road as a molecule.

Now since our molecules are patented, a competitor cannot use this road and hence would have to design a new road.

The road would have to be longer. The road may have to run through a mountain or a valley.

In effect it can never be as effective or as safe as the one straight road.

Add more roads to achieve destinations to reach the desired object. All straight roads being safe and efficient.

Very simplistic analogy

But pertinent to our molecules reaching and attaching to desired sites.

There are the Jak STAT pathways which in effect are roads in the molecular biological sense.

Signal transducer Activation of transcriptions.

Our molecules as they stand may will not be just limited to 1801 1802.

Aurora FLT3 l am certain were derived from the 30 odd molecules.

Indeed there was a problem of solubility which prevented entering the phase trials. Not that far apart from problems that TM stated in making our SDC 1801 1802 on a commercial scale.

Of 1.5 billion take a 10% pessimistic offer from a pharma in whatever form and that is still a 400 per cent rise from here.

I will not ramble on further, sumise to say that it would not be out of the question that the occupier of 737 may very well be invested in 1802 as both in field of oncology.

Views on dual therapy of 1802 and 737 and very likely Low dose Gemcitabine.

Welcome any debate on why this is not an option apart from 2802 has been given no definate target Indications.

Compounds are available to carry out preclinical work by different institutions.

Regards