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Been posted before, however just as a reminder
'We did not observe a significant anti-tumor 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+LDG with anti-PD-L1. All mice achieved some level of tumor regressions and 80% of mice (8/10) had complete tumor regressions which were sustained up to 60 days post treatment '
Triparna Sen
AZD1775 is a Wee1 inhibitor by AZ
We know that SO in their final trial design it was indicated
Sra737 plus either Parpi
SRA737 plus Wee1.
This from early 2022.
The other aspect here to take into consideration here is drug repurposing. In addition cost cutting.
It takes years and millions of pounds to bring a drug to phase1 trial.
Most of the drugs with their strengths and weaknesses are known.
It would be prudent to suggest that far more can be made in suitable drug in combo therapy, bu specialist organisations that result in a far more effective treatment as well as prolong the saleability of drugs in current commercialisation.
Then their comes the patent protection, and along with any new patent comes patent protection defeating the onset of generic drugs.
It gets complex.
Regards.
I doubt that very much.
Ad l see it the problem arises that in, in combo therapy more than 1 inhibitor is used.
Unlikely therefore that a large pharma would take on.
However, on the upside a research pharma being small can establish a most satisfactory in combo therapy with different owners of individual inhibitors.
A plus B and C work well in investigational.
Then from this there will be a need to trial on clinical trial.
Multi compound in combo therapy owned by different companies.
There will need to be an agreement whether in licence format or a contract of some sorts, to establish milestone payments and the future predicted values of this in combo therapy.
Sra 737 is ok as licenced to private pharma.
I am of the firm opinion of this private pharma is aiming to develop a satisfactory in combo treatment leading to commercialisation.
In this instance there will exist agreements/ permissions of somesort to allow clinical trial to progress.
Now we get to the point of funding.
Where does the funding originate from?
Is it supplied by a financial investor or finance carried out paid for by the owners of such as the PD-1 or Wee1 inhibitor for example.
This may be the main reason why the private pharma identity is not disclosed.
Just my thoughts on this one.
Small pharma can generate pre clinical investigational data on more than 1 combo therapy. Most likely they will already have this info.
On good data results the owners of the other inhibitors can be contacted to establish an interest xnd if so how much are they willing to pay upfront and and financial renumeration in detail.
Regards
Https://www.sciencedirect.com/science/article/pii/S2590098624000101
1802 is definitely the biggy in my view.
Interesting link below although from 2019
https://www.biopharmadive.com/news/meet-the-protein-responsible-for-nearly-100b-in-cancer-drug-deals/561097/
As much as we can complain on here there is absolutely nothing going to happen with SDC 1801 until full data results are released. That is the meat on the bone.
How we progress after these results are realised, we will be notified thereof.
Aussies have been good and expedient so far, as such not contemplating any unexpected delays. Sareum have money to pay the fees.
Ideally as l see it continue to phase 2a in Oz.
No bl00dy hold ups with our understaffed, overworked, inexperienced MHRA employees.
News can come anytime from.now until.end of H1.
Regards and enjoy the rise when it comes.
Good morning Bobbler,
Excellent post and an important link.
It maybe worthwhile noting thst Acrivon has been designated fast track in endometrial and breast cancer ( 2023). Prexasertib and IV admistered chk1 2 inhibitor.
https://www.cancernetwork.com/view/fda-grants-ftd-to-prexasertib-in-ovarian-endometrial-cancers
Future is very bright for Chk1 inhibitors in combo therapy. On its own it is effective in what it us designed to do but needs assistance from DNA damaging agents eg gemcitabine.
Regards
Just my thoughts on this one Potnak.
I would suggest that it may very well be that 1802 has a higher selectivity over Jak3 than 1801
As far as l can remember there was a Jak 3 inhibitor Ruxolitinib ( not sure if spelled correctly)
that was used and approved in some haematology cancers some years ago. I also am of the belief that it was to be approved for T ALL cancer just a few years back.
The point here is that whilst Jak3 may well be adept at cancers it does knacker the immune system leading to increased risk of infections.
Jak3 can only pair with Jak1.
I would suggest also along with T ALL cancer it may prove effective in colon or bowel cancer.
Now, UC and CD have a high tenancy to lead to colon or bowel cancer.
Such is the close link here between the 2 that dependant on severity 1802 may prove to have greater efficacy in UC and CD.
I may be off my nut, but is just my way of thinking on this.
Regards
More than likely will go to different partners.
SDC1802 may well prove very encouraging in auto immune. Whilst similar in the compounds there does exist a difference.
Bare in mind that 1802 was being tested in SLE.
It is not beyond probability that preclinical data on 1802 may well indicate areas of auto immune that 1802 would have greater efficacy in.
However, even if this was not the case, anybody that the licensed was obtained by, could not use the 1802 compound for auto immune conditions, without additional payment for the use of.
Had this patent not been obtained, in theory a licence owner could trial in Indications and may be obtain approval for clinical use in auto immune. In this case Sareum would receive no funds as not in the patent description.
My own personal opinion is that SDC1801 would lack efficacy on cancer. I may be wrong.
We have a point here with auto immune in that could 1802 prove competitive against 1801 on some auto immune conditions such as UC or CD?
We will get to know in time.
Regards
No adverse effects up to 300mg per day.
Thst on its own is satisfactory.
In addition we await PK and biomarker data which will give an insight as to the most promising Indications that SDC1801 is likely to have most efficacy in on top of Psoriasis.
With regards to value of SDC1801 it will depend on what other Indications it is likely to prove successful in, and this will require to a certain extent PK and biomarker data to give idea of Indications.
Interestingly a competitor as such is being tested in Alzheimers. Baricitinib a Jak1 Jak2 inhibitor.
Drug companies seem desperate in repurposing certain inhibitors.
Regards
No problem with solubility issues with 737.
Aurora +FLT3 had solubility issues with regards to the oral formulation of, not too far away from difficulties with Sareum on SDC compounds.
The SDC compounds difficulties encountered in producing compound in sufficient quantities for clinical trials require comparatively massive amounts as opposed to low levels in preclinical investigational work.
Regards
Being of a similar but not identical compound ie they are both Tyk2 and Jak1 SDC 1801 should progress to phase 2 trials.
Interestingly SDC1802 has now l believe have further patent protection in the area of auto immune.
Door should be wide open on decent data results.
Regards
Interesting.
'The second key difference between Phase Ia and Phase Ib clinical trials is the dosage of the drug administered. Phase Ia is the single ascending dose (SAD) study, wherein participants are given a single dose of the drug before close observation. If there are no notable adverse events, the expected pharmacokinetic activity is confirmed, and the dose can be escalated. This process is repeated until the maximum tolerated dose (MTD) is reached in human subjects. Once a third of all participants exhibit severe side effects with a particular dose, it is considered the MTD. In the event of adverse events occurring, the dose may also be decreased to reach the MTD.
In contrast, Phase Ib is the multiple ascending dose (MAD) study, which can offer more information with a faster route because these trials can simultaneously test multiple dosages all under one protocol. By comparing different doses across each treatment group, the researchers can easily compare the pharmacokinetics and pharmacodynamics at each of these doses.
More in depth in the link below.
https://worldwide.espacenet.com/publicationDetails/description?CC=EP&NR=2634185B1&KC=B1&FT=D&ND=1&date=20160113&DB=EPODOC&locale=en_EP
2.15 A compound of formula (2) or a salt thereof as defined in any one of Embodiments 1.38 to 1.105 for use in a method of treating a disease or condition in a subject in need thereof, wherein the disease is any one or more diseases or conditions selected from:
(a) skin inflammation due to radiation exposure;
(b) asthma;
(c) allergic inflammation;
(d) chronic inflammation;
(e) an inflammatory ophthalmic disease;
(f) dry eye syndrome (DES, also known as keratoconjunctivitis sicca or dysfunctional tear syndrome);
(g) uveitis (e.g. chronic progressive or relapsing forms of non-infectious uveitis);
(h) insulin- dependent diabetes (Type I);
(i) Hashimoto's thyroiditis;
(j) Graves' disease;
(k) Cushing's disease;
(l) Addison's disease (which affect the adrenal glands)
(m) chronic active hepatitis (which affects the liver);
(n) polycystic ovary syndrome (PCOS);
(o) coeliac disease;
(p) psoriasis;
(q) inflammatory bowel disease (IBD);
(r) ankylosing spondylitis;
(s) rheumatoid arthritis;
(t) systemic lupus erythematosus;
(u) myasthenia gravis;
(v) transplant rejection (allograft transplant rejection); and
(w) graft-versus-host disease (GVDH);which method comprises administering to the subject an effective TYK2 inhibiting amount of the compound of the formula (2)
Plenty to choose from
The added bonus Brighty1 is that an RNS announcement that we have been granted clinical phase 2 approval will raise the SP more than we are entering phase1b.
Regards