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I don’t agree with that Thoth as in past experience if the Nomad is unhappy then don’t they normally resign position and a company has a number of days to find another, I think Sareum need something new that WH Ireland does not offer as a service looking at the website on services there is a distinct difference between them both imo!
If you need tools to get the job done you have to have these services, we have just had a fund raise and I guess some dialogue from management would do wonders for long terms investors so could be something necessary in facilitating/advising/advancing, I feel it’s a positive step!
Must know info to know it has a similar profile or is that the meaning disease type!
This is a TYk2/JAK1 inhibitor, according to $GLPG's Q1 report. This would have a similar profile to $PFE's PF-06700841 and $SAR's SDC-1801.
I think we have reached a point that SRRA has protected itself with an insurance policy they can’t drop it as the molecule hasn’t failed but opposite but have released positive results that can be taken forward commercially but still want extra help in doing so (re-negotiate milestones) as a company that has had a kicking in sp as a perceived to be supposedly hard up of cash and can’t be raised to dilute but have $80m in cash! Hmm!
Just United States Phase 1 first dosing payment not Phase 2!
“including a milestone payment of $7.5 million upon the dosing of the first patient in the first Phase 1 trial of SRA737 in the United States, and a payment of $12.0 million upon the dosing of the first patient of a randomized Phase 2 trial of SRA737.”
If they didn’t pay phase 1 milestones so is deferred with the additional phase 2 payment now due of $19.5m and they want to renegotiate the payments!
“a milestone payment of $7.5 million upon the dosing of the first patient in the first Phase 1 trial of SRA737 in the United States, and a payment of $12.0 million upon the dosing of the first patient of a randomized Phase 2 trial of SRA737. In the event that the milestone payment for Phase 2 becomes due, but no milestone payment for Phase 1 has been paid, then the milestone payment for Phase 1 will become due and payable contemporaneously with the payment for the Phase 2 milestone for an aggregate payment of $19.5 million.“
It’s not a personalized RNS but they are pointing out the bits they feel relevant to us and legally the path forward for it!
I don’t think it’s all doom and gloom most info was known and I’m sure a few taking advantage of jumping on with negative comments!
The situation is to be negotiated as with the milestone payments of $19.5m due and Sierra want as much money to progress their momelotinib!
They have provided a clear path to registration with the trials and have spent a lot of money providing good data even if Sareum and CRT take back then it could be commercial good for us as most of the hard work is done with risk and SRRA could loose this and pay damages!
I don’t think they do want but I think they want to squeeze SAR’s and CRT’s balls to test the water and see what SAR and CRT come back at them with maybe threatening to take back could do some good, if they can get a reduced payment to SAR and CRT then they will most certainly try it, it’s business after all!
“If we breach any of these obligations, or use the intellectual property licensed to us in an unauthorized manner, we may be required to pay damages and the licensor may have the right to terminate the license”
Hang on a minute isn’t Stanford university the SRI at Menlo Park California?
With SDC-1801 being in competition with BMS (Bristol-Myers Squibb) Tyk2 inhibitor for autoimmune diseases and with 1801 synthesis manufacturing routes being completed but SDC-1802 further behind do you think that they will license SDC-1801 to a BMS competitor and use the cash to take the novel SDC-1802 for Cancer through too the clinic or further depending on how much money?
Aber can’t find a specific TYK2 for Cancer only one I think is Sareum’s SDC-1802 glad to be directed!
There’s the new research just being released for TYK2 in Autoimmune so this is a different story with BMS but any sign that SDC-1801 is on par with BMS-986165 then we will not be here, so a lot to be gained from the peer review that is being prepared!
Autoimmune pathways in mice and humans are blocked by pharmacological stabilization of the TYK2 pseudokinase domain
Tyk2 preclin paper from BMS, impressive work. H/T to @NimbusTx who we feel has quite a formidable Tyk2 inhibitor themselves
Promising New TYK2 Cancer Research, 18th June 2019!
TYK2 promotes malignant peripheral nerve sheath tumor progression through inhibition of cell death
Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive sarcomas that arise most commonly in the setting of the Neurofibromatosis Type 1 (NF1) cancer predisposition syndrome. Despite aggressive multimodality therapy, outcomes are dismal and most patients die within 5 years of diagnosis. Prior genomic studies in our laboratory identified tyrosine kinase 2 (TYK2) as a frequently mutated gene in MPNST. Herein, we explored the function of TYK2 in MPNST pathogenesis.
Immunohistochemistry was utilized to examine expression of TYK2 in MPNSTs and other sarcomas. To establish a role for TYK2 in MPNST pathogenesis, murine and human TYK2 knockdown and knockout cells were established using shRNA and CRISPR/Cas9 systems, respectively.
We have demonstrated that TYK2 was highly expressed in the majority of human MPNSTs examined. Additionally, we demonstrated that knockdown of Tyk2/TYK2 in murine and human MPNST cells significantly increased cell death in vitro. These effects were accompanied by a decrease in the levels of activated Stats and Bcl-2 as well as an increase in the levels of Cleaved Caspase-3. In addition, Tyk2-KD cells demonstrated impaired growth in subcutaneous and metastasis models in vivo.
Taken together, these data illustrate the importance of TYK2 in MPNST pathogenesis and suggest that the TYK2 pathway may be a potential therapeutic target for these deadly cancers.
Despite this fact, there was a very significant decrease in tumor burden, suggesting that there may be other cell death mechanisms at play in addition to apoptotic cell death. Nonetheless, the mice injected with Tyk2-deficient cells exhibited less weight loss and had an increased overall survival, further supporting targeting this pathway in MPNSTs. Future studies will be aimed at better understanding the mechanisms at play in vivo. As we move forward with evaluating this pathway as a viable therapeutic target, another important aspect of TYK2 signaling that cannot be ignored is that TYK2 does not act alone, but is rather in a receptor complex in which either JAK1 or JAK2 is also involved. Thus, drug development strategies will benefit from understanding which of the other JAK family members are important in MPNST biology. Future work will be aimed at identifying the most effective inhibitor from in vitro studies and then evaluating the in vivo efficacy of the most promising TYK2 inhibitors to test as a single agent and in combination therapies.
Turner Pope research note, apologies if posted already!
Links of SRA737+ LDG + Keytruda