I had posted about the Majestec 3 trials last week. I had met and spoke to a doctor who had run the trials in England. He was very positive about the results. His comment was these drugs make MM a condition we live rather than a terminal illness. He said it work on all type of MM withe exception of certain mutations. He said the average patient lived 17 years with this treatment. All very positive.

Since DarzFasPro is known to Killer our Critically Important Natural Killer Cells, I asked AI about Tecvayli - 1) Does it Kill Natural Killer Cels - it does not. 2) Does it Protect them against DarzFasPro - No it does not but the conclusion has good News.

There's plenty of Supplements that can help to Boost our NKCells, which DarzFasPro depends on for it to work. It's up to us to Protect our NKCells - our Innate Immune System. Oncs, Docs, and Specialists are Not Taught about Nutrition and many don't even know what Natural Killer Cells are (a subcomponent of our White Blood Cells) that can Kill Things that are Just Wrong, rather than being a Learnt Immune Response of our Igs).

No, **Tecvayli (Teclistamab) does not protect** your Natural Killer (NK) cells from being killed by Darzalex FasPro.

When used together, the depletion of NK cells caused by Darzalex still occurs.

### Why It Does Not Protect Them
1. **Different "Lanes":** Darzalex works by hunting for the **CD38** protein. Because NK cells are covered in CD38, Darzalex finds them and kills them ("fratricide").
2. **No Shielding:** Tecvayli binds to different proteins (**BCMA** and **CD3**). It does not cover up or "hide" the CD38 protein on your NK cells. Therefore, the Darzalex can still see and attack the NK cells just as easily as if you were taking Darzalex alone.
3. **Clinical Evidence:** Recent data from combination trials (like the MajesTEC-3 study) confirm that **NK cell reduction is still observed** in patients receiving both drugs together.

### Why The Combination Is Still Powerful
Even though you still lose your NK cells, the combination is considered "synergistic" (more powerful together) because they recruit different parts of the army:
* **Darzalex** handles the "cleanup": It depletes immunosuppressive cells (T-regs) and stresses the myeloma cells.
* **Tecvayli** brings in the "Special Forces": Since your NK cells (the first responders) are depleted by Darzalex, Tecvayli compensates by forcefully activating your **T-Cells** (the precision killers) and guiding them directly to the cancer.

**Summary:** You will likely still experience the drop in NK cells typical of Darzalex treatment, but Tecvayli helps bypass this loss by activating T-cells to do the heavy lifting instead.

Great news for us all 😀

@A MyMyelomaTeam Member,
I don’t think that is correct. That would mean any deletion, translocation, or addition would be extramedulary disease. It is true that MM is systemic, but if you don’t have lesions, tumors, or amyloidosis, then I would not worry.
Paula🌹

Mentioned Users

A MyMyelo...

Impact of High-Risk Features
While the MajesTEC-1 trial showed an overall response rate of 63% in heavily pre-treated patients, subsequent real-world data and studies have provided more nuance regarding high-risk features.
High-risk cytogenetic abnormalities: Patients with multiple high-risk chromosome abnormalities, such as del(17p) or t(4;14), tend to have less favorable outcomes and the disease may come back more aggressively when treatment is stopped.
Extramedullary disease: The response rate to teclistamab appears to be somewhat lower in patients whose multiple myeloma has spread outside the bone marrow to soft tissues or organs (extramedullary disease).
Prior BCMA-targeted therapy: Patients who had previously received other B-cell maturation antigen (BCMA)-targeted therapies (e.g., some CAR T-cell therapies) were generally ineligible for the MajesTEC-1 trial, and real-world data suggests a shorter progression-free survival in this group compared to those who had not.
The Role of Genetic Testing
Researchers are actively studying the genetic makeup of patients' cancer cells to better understand resistance. Identifying specific genetic changes can help predict which patients might not respond well to current BCMA-targeting therapies like teclistamab and guide clinicians in tailoring treatment plans to improve success rates.
For more information on multiple myeloma treatment and genetic risk, consider visiting the International Myeloma Foundation or Moffitt Cancer Center websites.