Fate Therapeutics Inc (FATE)

PR https://www.globenewswire.com/news-release/2026/06/04/3306754/24675/en/fate-therapeutics-showcases-data-from-ft819-and-ft839-programs-at-the-european-congress-of-rheumatology-annual-meeting.html+

Data https://www.fatetherapeutics.com/wp-content/uploads/2026/06/EULAR-2026_Poster_FT819-102-FINAL.pdf and https://www.fatetherapeutics.com/wp-content/uploads/2026/06/FT839_EULAR_2026_FINAL.pdf

PR https://www.globenewswire.com/news-release/2026/06/01/3304368/0/en/fate-therapeutics-showcases-clinical-data-for-ft836-at-the-american-society-of-cancer-oncology-annual-meeting.html

Poster https://www.fatetherapeutics.com/wp-content/uploads/2026/06/ASCO-2026_Poster.pdf

New deck https://ir.fatetherapeutics.com/static-files/eda64ddb-7bcc-4539-972f-cef267a099f2

Based on the poster, I don't think it is possible to determine the cause of the sepsis event. In heavily pre-treated mCRC patients, sepsis can occur for many reasons unrelated to the therapy itself.

What caused Sepsis without LD?

Based on the slides, NT-175 looks interesting. The slide that jumps out is in metastatic pancreatic ductal adenocarcinoma. Even with the very few patients treated, seeing multiple responses is noteworthy. Historically, that type has been one of the most difficult solid tumours for any therapy.

The ORR, DCR, (m)PFS, (m)DoR, and the fact that some responses appear ongoing is encouraging.

As for the failures, a lot barriers still remain even when persistence is largely solved. That is the kind of information that can often result in next generation versions.

A know a new version will add a CD8 co-receptor into CD4+ T-cells and knockout CBL-B as well https://aacrjournals.org/cancerres/article/85/8_Supplement_1/3478/758580/Abstract-3478-Pre-clinical-characterization-of https://jitc.bmj.com/content/13/Suppl_2/A396 https://clinicaltrials.gov/study/NCT06218914

Going forward, it should be possible for them to insert a single multifunctional DNA cassette into the TRAC locus with manufacturing improvements. For the former, they could add an optimised TCR, CD8 co-receptor (+/- co-stim domain(s)), cytokine signal(s), and additional modifications, such as shRNA to knockdown CBL-B and TGFRB2.

So far, so good. Eligibility required R/R disease, and at least three prior lines of therapy, including a proteosome inhibitor, an immunomodulatory drug, and an anti-CD38 mAb. All patients achieved a response, and responses deepened over time. The one patient with extramedullary disease showed complete resolution by month one. A lymphoma candidate is already in the works. I wouldn't be surprised if they expand to autoimmune diseases as well.

For solid tumours, I know of at least three companies developing ''armoured'' in vivo CAR-T therapies, including Waypoint Bio, which is leading the pack.

As for off-targets, still too early to say.

So far, a mixed bag. At future updates I'd want to see mono, paclitaxel-containing regimens, more KRASwt MSS mCRC patients, and patients with liver mets. Also, are any reductions/responses transient or durable. In addition, Day-22 biopsy analyses.

Adding lymphodepletion (despite the entire premise that it is not needed) chemo could improve the expansion and persistence of FT836 by creating "space" and reducing competition for homeostatic cytokines. The question remains if and how much efficacy is being sacrificed to avoid lymphodepletion. It would be easier to add conditioning later than to convince doctors and patients to accept conditioning if they demonstrate activity without it.

There are also rational adjuncts, including low-dose 5-FU, low-dose radiotherapy, low-dose panobinostat, and low-dose celecoxib. At least two of these would be straightforward clinically.

It is a sad day for cancer patients

BCMA TCE, biAb were great in MM too. Works great on plasma cell depletion. But SLE is not cancer, it is germinal centers driven by Tfh and LLPC. Invivo will be useless in solid cancers where T cells are suppressed, TCE, biAb, ADC are all useless. What is the chance of 0ff target editing that creates leukemic T cells?

An update: ''All 18 patients with relapsed or refractory multiple myeloma who have so far been treated with Kelonia’s KLN-1010 had no cancer in their bone marrow one month later, as determined by a test for minimal residual disease (MRD). All patients able to be assessed six months after treatment still had no cancer, and the patient with the longest follow-up—beyond 10 months—also remained MRD negative.'' https://www.fiercebiotech.com/biotech/asco-kelonia-keeps-vivo-car-t-momentum-rolling-nutty-100-response-rate

AI/ML is not good enough for MSS CRC. PDAC. You need ipsc cells with CAR/ good target, not autologous T cells from serum of 3L patients. Look at NT-175, the cells persist after 12 months. HLA downregulation made it useless after 6 in PDAC

The CD58 KO is one of the more differentiated aspects of what Fate is doing, while CD16A with the mAb has a clear rationale.

As for CAR design, Fate developed an AvER, which improved antitumour activity https://jitc.bmj.com/content/12/Suppl_2/A355

Also, AI/ML models can analyse data from massive high-throughput screens to predict how combinations will affect cell function, cytotoxicity, and persistence https://www.science.org/doi/10.1126/science.abq0225

Platforms like CAR-Toner have been developed as well https://communities.springernature.com/posts/harnessing-ai-to-refine-the-future-of-car-t-therapy-insights-behind-the-development-of-car-toner

The really interesting future is not just using AI/ML to optimise CARs, but optimising the entire engineered cell and phenotype for different cancers.

I no longer think the CAR design and lineage antigen selection will be as important as CD58 KO. The key is immune escape for the T cells in the highly suppressive MSSCRC. The beauty of FT836 is the lowered cell adhesion which minimize myeloid cell interaction and CD16A which increase tumor cells interaction thru Ab.

Thanks. For this trial, the primary endpoint is CRR (at week 26), which requires UPCR, eGFR, and no rescue therapy.

Based on the data so far, it suggests some patients achieve deep renal responses (that would be CRR), while the cohort overall showed broad renal improvement. It will be interesting to see the EULAR data looking at reproducibility across the cohort.

The CEO, Dr. Wang, disclosed for the first time that the dual-target CAR-iNK product NEUK203-215 for autoimmune diseases has enrolled seven patients with no SAEs to date, and all patients showed a successful immune reset in the peripheral blood. Except for the first low-dose patient whose response was close to the target, other patients treated with medium to high doses achieved or exceeded the present endpoints within up to three months.

Another CAR-iNK product for DLL3+ solid tumours, NEUK203-13, has been tested in the first patient, who demonstrated a good safety and tolerability profile. In addition, iPSC-derived iT and iMSC products have completed the development and validation of editing and manufacturing processes, progressing to preclinical evaluation.

They have also initiated in vivo CAR tech and product development, with early proof-of-concept for proprietary CD7 antibody-conjugated tLNP-specific delivery platforms.

Waypoint Bio has raised $20 million in a Series A financing to test multiple cell therapies in China.

They plan at least three IITs in China with this new funding round, which comes on top of an initial raise of $14.5 million https://www.businesswire.com/news/home/20240628087950/en/Waypoint-Bio-Launches-with-%2414.5M-to-Turbocharge-Drug-Discovery-using-in-vivo-Spatial-Pooled-Screening-Technology

Two of the CAR-T cell programs (both ex vivo and in vivo) will target Claudin 18.2 in gastric, GE junction and/or pancreatic cancers, and should begin by the end of the year. A third (in vivo) for CRC and prostate will be tested at a later date.

One armouring strategy it will use is a novel synthetic protein that boosts the infiltration of T-cells into tumours and, once inside, increases the proliferation and cytotoxicity.

Preclinical data https://aacrjournals.org/cancerres/article/84/6_Supplement/6329/735626/Abstract-6329-Pooled-in-vivo-screening-of-hundreds https://jitc.bmj.com/content/12/Suppl_2/A382 https://aacrjournals.org/cancerres/article/85/8_Supplement_1/3181/757112/Abstract-3181-Single-cell-characterization-and https://jitc.bmj.com/content/13/Suppl_2/A265

NK still works in AML , NHL based on AFMD trials data, not CRC, NSCLC ..................

I wrote off NK after NK engagers failed miserably compared to TCE. It can't even compete in AID, look at the dosages NKTX, ARTV use for RA. It is too lame

Newer work from the U of M suggests that transcriptional programming can improve iNK function https://academic.oup.com/jimmunol/article-abstract/214/11/2961/8239067

Also, the ''best'' engineered products may need to build on an tissue-resident adaptive phenotype, not bulk NKs. Again, recent data from the U of M https://aacrjournals.org/cancerimmunolres/article/doi/10.1158/2326-6066.CIR-25-1229/784908/Integrated-Single-Cell-Profiling-Reveals

The tissue-resident adaptive NKs were the only subset (out of six) that demonstrated consistent, robust associations with improved survival across different primary, therapy-naïve and metastatic solid tumours, and in response to checkpoint blockade. Notably, elevated infiltration of these NKs was more prognostic than high tumour mutational burden in certain types treated with checkpoint blockade. Additionally, these NKs were strongly correlated to the infiltration of CD8+ T-cells and B-cells in tumours. Interestingly, paired pre- and post- checkpoint blockade treated tumours revealed expansion of cytotoxic tissue-resident adaptive NKs after treatment.

The MICA/B intellectual property may be valuable, though the moat may ultimately come from engineering rather than the antigen target alone.

They can't finish P1 dosing study by June if they didn't focus on tumor type and regiment. MSS CRC and Cetuximab + FT839 was chosen before P1 started.

The HER2 arms don't necessarily imply cetuximab combinations are succeeding. Two of the Regimens were likely designed to test FT836 with the HER2 mAb in parallel, especially given the CD16 receptor. The stronger evidence will come from expanded cohort data (if it is presented in 2H): whether activity appears beyond isolated responders, whether mono FT836 show signals, and whether paclitaxel improve outcomes versus mAb combinations alone.

If the cetuximab combo failed in 3,4 pts, the logical follow up would be LD taxane regiment D arm, not the HER2 Ab arm. They are not trying to prove Abs still work as salvage therapies

If true (about all nine), that would matter because the early efficacy signals could mostly reflect combination activity, not FT836 monotherapy, so it becomes harder to infer whether FT836 alone contributes meaningfully.

As for LD chemo and RT, true, but the current protocol has a number of arms, including with paclitaxel, which suggests they think tumour/TME preparation may matter.

Also, the HER2 arms may exist because of different populations and a broader commercial opportunity.

For the OV trial just canceled, pts must have received prior bevacizumab. They want an intact BBB in GBM pts to see the impact of CAR mica/b only

They shut down the FT536 trial on ovarian cancer. The GBM trial is to see the impact of mica/b CAR on CNS lesions and safety.

Many bios including ones in China can make ipsc NK. I don't see much value there. I think it is the CAR they are interested in, Dana-Farber Cancer Institute holds the mica/b trunk patent.

Opening this trial suggests continued institutional confidence in the broader platform and safety profile, but for an academic trial it looks unusually conservative looking at the number they plan to enrol and the (primary) endpoint. As for the exclusion criteria (prior bevacizumab or cellular therapy), it could reflect concerns around immune effects, confounding interpretation, wound healing, and/or edema.

I think the trials (including another in recurrent ovarian, fallopian tube, and primary peritoneal cancers also using FT536) will feed directly back into the next-gen iPSC engineering strategy that the U of M has a number of grants for like this https://reporter.nih.gov/search/d9lW8yEhyEKJeSffPzNN6Q/project-details/11158564

''Results:

First three pts (all MSS mCRC; median: age 45 y, prior therapies of 5, disease duration of 51 months) were treated in Regimen C dose level 1 (DL1 = 300 million cells/dose, Days 1 and 15 with cetuximab, no CCT) and completed dose limiting toxicity (DLT) evaluation (data cut-off 15 JAN 2026) with no DLTs, FT836-related serious adverse events, cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), or graft-versus-host disease (GvHD) reported. One of the three pts demonstrated a CEA response with >50% reduction (480 ng/mL at BL; 230 ng/mL at 4 weeks after first FT836 infusion) that correlated to mass shrinkage in all target lesions in a week 7 CT scan (obtained after data cut-off date). Of the other two pts, one experienced PD while the other was not yet assessed at the time of abstract submission.

FT836 was detected in peripheral blood (PB) following the first dose, with persistence observed up to 1 week. Notably, FT836 cells were detected beyond the initial PB detection in a tumor biopsy obtained at Day 22 (±3 days) indicating greater persistence in tissue compared to PB, supporting the value of additional engineered elements. EGFR and MICA/B antigens were identified in 3/3 baseline tumor biopsies, highlighting the relevance of multi-antigen targeting in driving patient outcome.''

All 9 pts are FT836 + cetuximab except 1. There is no need for LD chemo or RT. If cetuximab combo failed, they would have tried the triple combo, not HER2 Ab. U of M would not start another GBM trial with FT536 if targeting mica/b trunk failed in MSS CRC. Watch what the institution doing, why bother with CNS lesions if peripheral lesions didn't respond

Abstract is out today. I'm not expecting much (in it), but when the data is presented I will be looking to see if there is activity in those with liver metastases and as a single agent. Also, if paclitaxel adds anything, does an antibody help, and does the triple combination outperform.

Looks like U of M is preparing to treat MSS CRC pts. with CNS lesions. The OR they saw in pts without CNS lesions must be significant. They are using FT 536 in GBM pts as POC.
Exclusion: Received prior treatment with bevacizumab or any other cellular therapy available on or off a clinical trial.

My guess is 8 to 9 patients will be MSS CRC, 8 EGFR, 1 HER2

This new update is going to be more informative, but it still will be a small cohort, especially spread across multiple regimens, including Regimen C (cetuximab combo) and Regimen E (trastuzumab combo). So far, safety remains the strongest story. A key question will be if the first CRC signal is reproducible.

selective depletion of pathogenic immune cell subtypes in RA and SLE disease samples, including over 99% of B cells, plasmablasts, and plasma cells and more than 90% of activated CD4+ and CD8+ T cells, while sparing non-activated T cells

Pivotal starting 7/1/2026

FATE bio beast set up

Sword only depletes high 4-1bb+ cells, Dr. V mentioned that in presentation. You can check the poster on 836 to see this There is not many activated effectors in MSS CRC anyway unlike NSCLC. CD58 KO also raise the threshold for sword to deplete most immune cells activated.

I think it will be a standard poster showing initial safety and signs of activity. The interesting part will be the biology (no conditioning +/- combo with mAbs), but this is more proof-of-mechanism.

4-1BB is upregulated on activated CD4+ and CD8+ T-cells, as well as NK cells. So the ADR wouldn't just deplete (a subset of) Tregs, it could also affect activated antitumour T-cells and/or NK cells. Hopefully, they will look at this and present data in the near future.

IT = CXCR2
another Treg depletion
https://www.nature.com/articles/s41586-026-10341-w

Early pharmacodynamic evidence across three different trials in China (two in autoimmune* and one in haematological malignancies) show that in vivo mRNA CAR approaches can induce systemic CD19+ B-cell depletion across compartments (blood, LN, and/or BM), but still without sufficient numbers to determine safety, durability, and long-term clinical benefit.

* Being presented at the upcoming ASGCT conference.

The sword also deletes Treg like CTLA4 Ab. Cetuximab just clothes hanger for 836

Agreed, heterogeneity across lesions is real, but I think this argues for combination mechanisms rather than against them. If anything, heterogeneity makes a multi-mechanism approach like this (of the CAR plus ADCC) more plausible than a single-agent effect.

That they had both reductions in LDH and CEA is a strong early signal, but not unprecedented with effective therapy - just uncommon in (late-line) mMSS CRC. This an early systemic readout of cancer cell targeting and tumour shrinkage.

Why RECIST can favor TKI-like responses
1) Size-based measurement

RECIST 1.1 mainly measures change in lesion diameter.

TKIs often cause:

quick shrinkage of driver-dependent lesions
noticeable radiographic responses within weeks

That translates directly into:

partial responses (PR)
higher ORR
Slow immune remodeling is undercounted

Therapies like:

Pembrolizumab
cell therapy
some antibody combinations

may produce:

delayed responses
stable disease first
pseudoprogression
uneven lesion responses

RECIST can undervalue these patterns.

Upcoming at ASGCT:

CAR T cells Targeting pan-Tumor Antigens MICA/B can be Uniquely Combined with SOC Treatments without Conditioning Chemotherapy for Broad and Effective Therapeutic Application in Cancer https://pag.virtual-meeting.org/US/asgct2026/en-US/pag/presentation/686086

Upcoming at EULAR:

Safety and Efficacy of an Off-the-Shelf Anti-CD19 CAR T-Cell Therapy With Reduced Conditioning in SLE: A Phase 1 Study Supporting Same-Day Discharge https://pag.virtual-meeting.org/EULAR/eular26/en-GB/pag/presentation/24303


Off-the-Shelf Dual-CAR T-Cell Therapy: Targeting B and T Cells in Autoimmune Disease Without Preconditioning https://pag.virtual-meeting.org/EULAR/eular26/en-GB/pag/presentation/24009

3 pts and ASCO. what is brewing?

Preliminary phase 1 results of a MICA/B-targeted CAR T cell designed to overcome solid tumor escape mechanisms and avoid the requirement for conditioning chemotherapy.

January 27, 2026
Abstract Submission Deadline
abstract will be available on May 21 at 05:00 PM EST.