Incidence of pseudoprogression for immunotherapy appears slightly higher in melanoma as well (below) - maybe there is something about melanoma that promotes pseudoprogression. I would recommend not making the mistake of using the best case scenario in your modelling for a biotechnology company. The drug development process is extremely difficult because biology and particularly cancer is hard. The posters here who crack on about RAC being a has-been are a prime example of stupidity. Established clinical efficacy in humans is so extremely valuable because 97% of all compounds that make their way to the clinic fail to show anything meaningful. Reformulated drugs have an 80% success rate. There is a fair margin between 80% and 3% success rates.
There are many of examples of reformulated drugs being a clinical and commercial success in oncology:
Inqovi - reformulated decitabine
https://www.taihooncology.com/us/news/2020-07-inqovi-approval/Enhertu - reformulated herceptin
https://www.astrazeneca.com/media-centre/press-releases/2024/enhertu-improved-pfs-in-her2-low-and-ultralow.html
Table data taken from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6936240/pdf/cbm-16-4-655.pdfWhere is the evidence that supports increasing the dose improves clinical efficacy? You have access to CF33 clinical data now as well as other oncolytic viral therapy studies, so show me exactly where you are drawing your information from. Based on the preclinical data referenced by IMU, CF33 should already be outperforming the competition. Why are you saying increasing the dose should improve efficacy, when IMU specifically state that you need 2-5 orders of magnitude
less CF33 than other
competitor viruses (below)? The issue is the wording used by management and the way in which posters of this forum
erroneously interpreted the data. Parental viruses are essentially the backbones of products like CF33. They have not gone through an optimisation process for killing cancer cells, while compounds like CF33 have. Comparing an engineered compound (CF33) to a backbone parental virus is like comparing a showroom car to the warehouse chasis.
Since you like comparing apples to apples, why are you making the statement that CF33 outperforms T-VEC preclinically, when IMU report a single
lung A549 xenograft model, where
T-VEC has never been tested clinically and is approved for use in Melanoma. Are you seriously going to extrapolate from a xenograft cancer model where T-VEC has never demonstrated efficacy, state CF33 outperformed T-VEC preclinically, and as a result suggest the
reasonable thing to presume is that this is grounds for expecting an improvement in efficacy? As of Dec 2023, 3 people with lung cancer had received CF33 with 0 reported responses.
Despite many attempts, I have never found published peer reviewed literature that supports "
Preclinical data has demonstrated that CF33 is more efficacious than all parental viruses and
most viruses in clinical trials".
The CF33, GLV-1h68 T-VEC A549 xenograft model comparison was not included in the lung cancer publication:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170804/The CF33, OncoVex, and GLV-1h68 BXPC-3 pancreatic cancer in vitro comparison was not included in these pancreatic cancer publications:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8896143/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8787938/https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-018-1483-x
The reality is that IMU have sold investors misinformation. The majority of respsected posters on this forum have exacerbated this problem because they do not know the science and have no depth of scientific rigor. I have maintained a balanced, critical contrarian view that has been extremely accurate. Investors can see me as the enemy all they want, but I didn't sell them CF33 or HER-Vaxx.
(20min delay)