Replies to post #697293 on NorthWest Biotherapeutics Inc (NWBO)

[JFR161162]

Theo, you seem nervous all of a sudden.

[dstock07734]

We don't need to wait for SIO's filings in mid-August. I can tell you now.

The board has been talking about the significance of SIO investment. What I am really curious about is what could possibly bring SIO to NWBO. I read the dissertation of the researcher in SIO, the only one who has the Ph.D. in in Molecular and Cellular Pharmacology. The gentle man is an expert in the field of small molecule inhibitor related to the modulation of t-cell function which may explain why SIO recently opened a position in Tyra in the past first quarter, a company trying to develop small molecule drugs, like FGFR inhibitor. Is it possible that when he was doing DD on Tyra and reading peer-reviewed publications on FGFR and its inhibitors he bumped into DCVax-L?

For instance, papers like the following which mentioned about both DCVax-L and FGFR. I think the answer is highly possible.

https://pubmed.ncbi.nlm.nih.gov/31106606/
https://www.spandidos-publications.com/10.3892/ol.2022.13632
https://www.mdpi.com/1422-0067/23/10/5351
https://www.mdpi.com/2072-6694/15/17/4279

Do you still think SIO is not a serious player? I can guarantee you SIO is a very serious player. Every share they are buying now will turn into a gold bar later.

Here is something from ChatGPT on FGFR inhibitor. You may read it for fun.

FGFR inhibitors can help overcome immunosuppression in the tumor microenvironment and enhance anti-tumor immunity through several mechanisms:

Reduction of Tumor Cell Proliferation and Survival: By inhibiting FGFR signaling, FGFR inhibitors can reduce the proliferation and survival of cancer cells, making them more susceptible to immune cell-mediated killing. This can decrease the overall tumor burden and potentially expose more tumor antigens to the immune system.

Modulation of Cytokine Production: FGFR inhibitors can alter the production of cytokines and growth factors within the tumor microenvironment. This can lead to a reduction in immunosuppressive cytokines (like TGF-ß and IL-10) and an increase in pro-inflammatory cytokines that promote immune cell activation and infiltration.

Reduction of Immunosuppressive Cell Recruitment: By disrupting FGFR signaling, FGFR inhibitors can decrease the recruitment and activity of immunosuppressive cells such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) within the tumor microenvironment. This reduction can relieve immune suppression and enhance the anti-tumor activity of effector immune cells.

Enhanced Immune Cell Infiltration: FGFR inhibition can lead to changes in the tumor vasculature and extracellular matrix, improving the infiltration of immune cells into the tumor. This increased infiltration can boost the effectiveness of the immune response against the tumor.

Synergistic Effects with Immunotherapy: FGFR inhibitors can be combined with immune checkpoint inhibitors (such as anti-PD-1/PD-L1 or anti-CTLA-4 antibodies) to enhance their efficacy. By reducing the immunosuppressive environment, FGFR inhibitors can improve the responsiveness of tumors to immunotherapy, leading to better clinical outcomes.

Downregulation of Immune Checkpoint Molecules: FGFR inhibitors can decrease the expression of immune checkpoint molecules like PD-L1 on tumor cells, making them more susceptible to immune attack. This can enhance the effectiveness of immune checkpoint blockade therapies.

Overall, by targeting the FGFR pathway, FGFR inhibitors can help remodel the tumor microenvironment to be more conducive to an effective anti-tumor immune response, thereby overcoming immunosuppression and improving the efficacy of cancer treatments.