Satri-cel is an autologous CAR T-cell therapy targeting the CLDN18.2 protein, which is expressed in certain gastric cancers.
The therapy has shown promising efficacy in heavily pretreated patients, with significant improvements in progression-free survival (PFS) and overall survival compared to standard treatments.
Patients lived about 40% longer on average, and tumor shrinkage was observed in a higher proportion of patients.
Before receiving satri-cel, patients undergo a conditioning regimen of fludarabine, cyclophosphamide, and nab-paclitaxel (a chemotherapy drug).
This is intended to deplete immune cells and create a favorable environment for CAR-T cells to expand and attack the cancer.
Ok the relevance to CHM’s CDH17.
CDH17 is a 3rd generation CAR-T cell therapy targeting CDH17, a biomarker associated with poor prognosis and metastases in gastrointestinal cancers.
The ongoing Phase 1/2 trial is for patients with advanced, relapsed/refractory GI cancers.
The protocol allows for bridging chemotherapy if needed for disease stability during manufacturing, but not within 2 weeks of leukapheresis (cell collection) or planned CAR-T infusion.
The standard pre-infusion regimen for CHM-2101 is lymphodepleting chemotherapy (LDC), typically with agents like fludarabine and cyclophosphamide, but not nab-paclitaxel.
Satri-cel’s use of nab-paclitaxel in the pre-infusion regimen is notable because nab-paclitaxel is a chemotherapy drug, not a standard part of most CAR-T pre-infusion protocols.
CHM-2101’s regimen is more “pure” CAR-T in the sense that it does not incorporate nab-paclitaxel in the pre-infusion phase.
The use of nab-paclitaxel may help to further deplete the immune system or sensitize the tumor, potentially enhancing the efficacy of CAR-T therapy.
Some investors may question whether the impressive results are due to the CAR-T therapy itself or the combination with additional chemotherapy, which could complicate interpretation of the data.
Is this positive for our Company?
If CDH17 achieves strong results without nab-paclitaxel, it could be seen as a more “pure” demonstration of CAR-T efficacy, which might be favorably viewed by the FDA EMA etc.
The opposing view is if nab-paclitaxel is shown to be beneficial, CHM could consider incorporating it into future protocols to further boost efficacy.
But,
The safety and tolerability of combining nab-paclitaxel with CAR-T therapy must be carefully evaluated.
Are the observed benefits due to CAR-T, chemotherapy, or the combination.
So in conclusion I will ask this. Let's say the Satri cells kill the cancer cells expressing the CLDN18.2 protein and increases PFS. That is great, but they are not targeting CDH17 protein cancer cells and the patient relapses. Horses for courses. The answer is why CHM is developing gene therapy to isolate our patients to give the best available drug.
In my view it's parallel competition. Good on them. Let's catch up to their PFS. We shall !
Kpax
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