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How CAR NK bios address this issue? NK can grab PD-L1 too.
Trogocytosis-based generation of suppressive NK cells
https://www.embopress.org/doi/full/10.1038/sj.emboj.7601570#:~:text=Trogocytosis%20is%20a%20fast%20uptake,targets%20material%20exchange%20is%20unclear.
Most bios are expensive experiments done by expensive PhDs. They are Wall St. shows nobody should stick around for the endings.
Yes. Signet-ring, TP53. ... dying. Even more aggressive than the ones enrolled in CART trial
$AFMD 24+ ATEZO was pretty effective (1/1) compared to CARThttps://t.co/WtuFoQNM37
— Bon Wood (@ny1972_47) September 28, 2023
More targets better than less. Frameshift mutations matter the most. Targets not enough if T cells getting exhausted anyway. They need a process similar to LuminICE
DTIL founders never worried about cash until the meltdown. They hired too many PhDs, built fancy expensive labs with lots of promises. They never tried to trim the expenses to make sure there will be cash left for clinical trials. High burn and lots of GT bios spell doom for this bio.
Innate immunity is a team sport. All these CAR NK bios want to do 1 on 1. How the gene edited NK cells behave in the heterogenous TMEs will make the trials more a learning experience.
IECure will buy the ARCUS IP when cash is 0 in 18 months.
this is a homeless shelter for PhDs. Cash is not spent on patients. They hired a chief people officer to cut the pie.
I gave up on all gene modified ACTs once I found out the price to pay is the capacity to interact with M2, B, T and ... in the TME. CART and CAR/NK look like a cell based ADC to me.
Allo CAR T/NK not going to be durable without engaging endogenous innate cells
https://www.cell.com/cell/fulltext/S0092-8674(23)00642-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867423006426%3Fshowall%3Dtrue
Efficacy and cost. With CBNK, there is less worry on IFN gamma expression and CD16A compared to AUTO PBNK. $2K per 2B allo cells from Artiva. Cheap
A lot of old CARs will be abandoned on the road. CARs sold by Wall St.
Didn't they buy TRIL? Just gambling with billions from US government.
With all the edits, CAR NK is more like ADC, not NK cells that have also been described as ‘immune-regulatory’ because of their ability to produce an array of cytokines and chemokines, through which they help shape B cell and T cell responses, and impact the function of DC, macrophages and neutrophils
CART is like a big bomb while carpet bombing with bomblets is needed to rid cancer everywhere in the body.
I like the LD before CBNK+ ICE+IL-2 combo. Targeted immunotherapy
FATE's targets BCMA, CD19,.HER2.. make it not investable. Too many ACTs, ADCs targeting the same.
GMO is no match to organic NK.
Not counting CART relapsed saved by CD13 +CBNK, AB 101 +CD20 also saved
3 of 4 pts who failed prior CAR-T therapy.
Why NKTX is not targeting cervical cancer?
NKTX could start by testing NKX101 in HCC, intrahepatic cholangiocarcinoma, and/or surgically resected CRC where only liver metastases remain via locoregional delivery.
Why endometrial cancer? High TIL + high NK?
Two PRs (pending confirmation) were observed in patients with endometrial cancer, one whose cancer had progressed on prior checkpoint inhibitor therapy
All these GMO cells is no match to CBNK. Artiva AB 101 shines with IL2 + CD20
Disfunctional NKs have a few more mutations than dysfunctional NKs.
My point was MDS patients has disfunctional NK cells which cause the cancer to slow down on MICA expression. With lowered MICA expression, NKTX cells don't work. I doubt MDS TME is more suppressive than AML.
It will be interesting to see how this DT HER2 x NKG2D x CD16A engager works since it won't be impacted by the # of ligands on cancer cells.
Cancer is adapting. Why bother expressing ligands if the NK cells are not working anyway.
NKG2D surface down-modulation in freshly isolated NK cells from MDS patients may be a clinically useful “biomarker” of suppressed NK function.
This one is puzzling. Four patients with MDS were treated, with no response observed.
CGEM MICA/B good enough for a poster. So much for the pan cancer claim. Not good news for NKTX.
A phase 1 dose-escalation study to investigate the safety, efficacy, pharmacokinetics, and pharmacodynamic activity of cln-619 (Anti-MICA/B antibody) alone and in combination with pembrolizumab in patients with advanced solid tumors.
Here is 1 reason why CSO left. Looks like ALLO is a bunch of born losers.
agct presentation from Novartis showing KO of endogenous TCR is deleterious to CAR-T function [269]; corroborates some academic work that was released previously
How much cancer risk is acceptable?
Looking at 250 mil burn, FATE and other bios like NKTX in the west will not survive.
PhDs love stock options from new bios. The bio bucks from retail investors made them muti-millionaires.
AFM28 - ADCP.
Some CEOs won't even PR. AFMD was a tool company so learning to cure will be tough sledding. I will take the working ICEs over some nice CEO any day. If you look at ASCO release today, there will be some nice nuggets coming from SAR443579. a trifunctional Natural Killer Cell Engager (NKCE) targeting the CD123 tumor antigen on cancer cells. I guess 30% ORR got the NKCE the oral session. It looks like AFM24 - ADCP.
This target must be older than 1/2 USA population
If you listen to DTIL CSO who just left, single edit is 19A/B key advantage
TME is poorly understood. Mgt. is crossing a fast moving river with eyes closed. They will adjust the strategy. ICE are active in AITL and gastric cancer based on latest data, which made sense since cancer bought up by EBV or H Pyloric are more antigenic by nature.
Endless edits still doesn't address the infection that started the mess. Viral or bacterial
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9289786/
What is the impact of multiple edits on NK longevity? Sounds like the cancer ligands are exhausting the CAR NK in PB before they get into TME.
"survival of transferred human NK cells is limited in NSG mice, and only a small number of human NK cells infiltrate lung tissue"
Another bio with endless research in crowded field, can't beat AUTO, can't salvage AUTO relapsed. Just lots of hype from crispr to keep printing shares.