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I reckon Aber if that were the outcome we would see a around a pound a share pre consolidation price. Circa market cap of 3 billion is not out of the question.
if all continues well on SRA737 alone, just prior to commercialisation should put us around the 400 million market cap.
Just my thoughts of ball park figure and there are others on here far more knowledgeable than me who can give a more reasoned case for a figure.
A while away and exactly how far, well who knows?
Be good also for those here that bought at a peak to get a decent return. They deserve it too.

Regards

BB. Yes looks like we differ in our opinions.
No Good GSK approaching CPF as agreement is between Sierra Oncology and CPF. I have not looked at the license agreement in years. If there were a problem with on licensing, prior consent could and may have already been granted.
agrrements are made to protect the interests of the original parties who were in agreement. One side cannot unilaterally change any terms of the agreement without the consent of the other party. The milestone reduction was agreed by both parties so things can change. There was much talk when Sierra Oncology ( formerly Pronai Therapeutics ) took on the license and perhaps who they could on licence to. However, it is such that Sierra oncology cannot do just as they like with the licence agreement. The only realistic way it would return to the CPF is by default. Sierra have well delayed development but as yet not to justify costly legal action by both parties. No one wants or will benefit from that and all including the compound become tarnished.
My belief is development of SRA737 will gather rapid pace not to sell on but to use in combination with GSK inhibitors ie PARP and PD1. With a little understanding of the research carried out and the workings of the compounds themselves I am sure you are aware of the massive advantages in retaining the CHK1 inhibitor.

I have not been here long and just my view of the situation

If you care to take a look at the RNS around March 2020 you will see the following paragraph

'SRA737 was discovered and initially developed by scientists at ICR in collaboration with Sareum, and with funding from Sareum and Cancer Research UK. SRA737 is licensed to Nasdaq-listed Sierra Oncology Inc. (“Sierra”) and has demonstrated positive safety and efficacy in combination with low-dose gemcitabine from a Phase 1/2 clinical development programme supporting standalone development in anogenital cancer. This programme is ongoing, with Sierra seeking to on-license SRA737 for further development.'

Note the 'Sierra is seeking to on-license SRA737 for further development'

ful RNS link is here
http://www.sareum.com/news/press-releases-and-news/2020/new-sra737-combinations-cancer/

Regards

The compounds of the invention are selective TYK2 inhibitors and are considerably more active against TYK2 than JAK2 and JAK3 kinases. The compounds have relatively poor activity against a wide range of other kinases and, in particular, kinases that are generally recognised as targets for anti-cancer therapy. Thus, for example, the compounds have relatively little activity against Chk1 kinase, Aurora kinases, PKB (Akt) kinase and cyclin dependent kinases (CDK kinases) which are involved in cell cycle progression. A lack of activity against kinases typically considered to be anti-cancer targets is beneficial in compounds that may be used in chronic treatment of inflammatory and autoimmune diseases for example.
It is envisaged on the basis of their TYK2 inhibiting activity that the compounds of the invention will be useful in treating at least some of the diseases and disorders discussed below, including inflammatory diseases or conditions, immunological diseases or conditions, autoimmune diseases, allergic diseases or disorders, transplant rejections (allograft transplant rejections); Graft-versus host disease; treating sepsis and septic shock.
In the context of the present invention, an autoimmune disease is a disease which is at least partially provoked by an immune reaction of the body against its own components, for example proteins, lipids or DNA. Examples of organ-specific autoimmune disorders are insulin- dependent diabetes (Type I) which affects the pancreas, Hashimoto's thyroiditis and Graves' disease which affect the thyroid gland, pernicious anemia which affects the stomach, Cushing's disease and Addison's disease which affect the adrenal glands, chronic active hepatitis which affects the liver; polycystic ovary syndrome (PCOS), coeliac disease, psoriasis, inflammatory bowel disease (IBD), lupus nephritis (an inflammation of the kidney) and ankylosing spondylitis. Examples of non-organ-specific autoimmune disorders are rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, and myasthenia gravis. Type I diabetes ensues from the selective aggression of autoreactive T-cells against insulin secreting beta-cells of the islets of Langerhans. Other inflammatory or immune diseases and disorders, sufferers from which may benefit from treatment with the compounds of the invention include skin inflammation due to radiation exposure; asthma; allergic inflammation; chronic inflammation; an inflammatory ophthalmic disease; dry eye syndrome (DES, also known as

From Journal of Thoracic oncology
Pimarily SCLC

Dec 2019 The SRA737 þ LDG
regimen mimicked the schedule currently being used in the clinical trial described above with or without anti–
PD-L1 on the third day of a weekly cycle. We did not observe a significant antitumor effect with any single agent treatments (anti–PD-L1, SRA737, or LDG), and only a moderately delayed tumor growth with combined
SRA737 and PD-L1 treatment (Fig. 4A). However, we observed remarkable tumor regressions when we combined SRA737 þ LDG with anti–PD-L1. All mice achieved some level of tumor regressions and 8 of 10 (80%) mice had complete tumor regressions which were sustained up to 60 days post treatment.

Here we show that the SRA737 þ LDG regimen in combination with anti–PD-L1 enhances dendritic cells in the tumor and leads to a decrease in pro-tumorigenic MDSC populations. Most notably, the establishment of the strong antitumor immune microenvironment observed when SRA737 is combined with low-dose gemcitabine opens an opportunity for a highly efficacious and tolerable treatment regimen with a potentially distinct mechanism from that
of standard chemotherapy or DDR inhibitors alone.

Further studies are warranted to determine if this approach would be beneficial with other chemotherapies, such as low-dose platinum-based doublets, in combination with ICB and DDR inhibitors. Whereas the RPP SCLC model used in the immune-competent animal experiments represents only part of the heterogeneity of
SCLC, our previous work with olaparib and prexasertib in combination with anti–PD-L1 suggests that our observations are more broadly applicable to SCLC.8,12,23 As with many other cancer types, pre-clinical studies are limited to only a few immune-competent models of SCLC, consequently further validation of the combinations described here, will likely need to take place in a clinical setting. Given that anti–PD-L1 drugs have recently been approved as monotherapy and in combination with chemotherapy for the treatment of SCLC, and that the SRA737 þ LDG regimen is well tolerated in clinical trials in SCLC (NCT02797977), our preclinical data provide a strong rationale for combining this regimen with inhibitors of PD-1/PD-L1 pathway in the clinic.

Termination of trial.
Would hazard a guess at financial issues especially comittment with the Momo. from memory Sierra were robbing the SRA737 cash pot to press ahead with momo. Around about 2 million dollars I believe cut back on SRA737.

EudraCT NumberFull title of the trialSponsor name2017-004927-56A Phase 1b/2, Open-label, Multicenter, Dose-ranging Trial to Assess the Safety, Tolerability, Pharmacokinetics, and Preliminary Antitumor Activity of SRA737 in Combination with Niraparib in Subjects with Metastatic Castration-resistant Prostate CancerSierra Oncology, Inc.
This study was prematurely terminated due to a change in the positioning of the clinical development pipeline for Sierra Oncology. The clinical trial was approved, but it was never started, no subjects were enrolled, and no clinical trial results are available.

A note i will add here is CHK1 is used in combo with LDG. Low dose gemcitibine as gemcitibine toxicity is high when used in higher dose with CHK1 inhibitors.

Masses of potential here. Effectively much more potential in combo. Much much more if we look at possibility with a TYK2 Jak1 cancer treatment. A question now exists of whether DDR will still need to be addressed when treating patients with ovarian cancer or similar forms of cancer that have known DDR pathways for example with a Tyk 2 inhibitor.
I believe it important as a whole not to think as inhibitors as one cure for all. It is in the contribution they can make in multi pronged attacks on cancer. This is where the true value lies I believe.
GSK are very heavily committed to development down this route. they are hell bent on research and development into IO ( Immuno Oncology). Certain inhibitors and treatments in combo will be required to maximise the potential for their already made treatments in clinical use and development.
Our SDC1802 is designed to be not only compatible with other treatments but also enhance their effectiveness when cancers develop resistance to earlier forms of treatment.

I would certainly not rule out a GSK sareum agreement of some sort with regards to our TYK2 Jak1 compounds. But we are a little way off and need indications of toxicity results in human trials. If results turn out as good as we have been led to believe then game on.

Beer oclock for me now.

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