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Any CAR. Any delivery. One signaling layer.

NanoKar is an optimization layer for existing CAR-T therapies, not a competing CAR-T. Our ITAM tuning platform addresses the persistence and toxicity barriers limiting the field today. Solid tumors are the open field in cell therapy, and calibrated signaling is how cell therapy gets there.

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100%
Survival Across Five Serial Tumor Re-Challenges (CD19 Model)
Any CAR
T Cell, NK Cell, Macrophage and More
Any Delivery
Ex Vivo and In Vivo
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How it works

A two-minute explainer: what a CAR is, what an ITAM does, and why NanoKar is the optimization layer for any CAR.

Every approved CAR-T carries the same CD3ζ signaling domain. One fixed sequence, never engineered. NanoKar engineers it. 26 tunable ITAM variants let activation be calibrated rather than fixed, shifting T cells toward memory instead of exhaustion. Nothing else about the construct changes.

Toxicity caps the dose. Dose is what solid tumors demand. Calibrated signaling widens the window at the source, and it travels with any CAR, any cell type, any delivery, with no change to targeting, co-stimulation, manufacturing, or regulatory path.

The Field Inherited One Signaling Domain

Every FDA-approved CAR-T therapy uses the same intracellular CD3ζ signaling domain sequence. That single design drives the three problems limiting the entire field: limited persistence, severe toxicity, and failure in solid tumors. Calibration runs in both directions: the variant library spans weaker and stronger signaling than the native domain, so potency can be raised or lowered depending on the program.

The Challenge
Our Solution

Limited Persistence

Short-lived CAR-T cells allow cancer to escape treatment. 30-60% of hematological malignancies relapse after current CAR-T therapies.

ITAM-Optimized Persistence

ITAM-optimized CAR-T cells generate long-lasting memory T cells with reduced exhaustion markers (PD-1, Tim-3, Lag-3). In a CD19 model, ITAM optimization produced durable tumor control across consecutive re-challenges versus the same CAR carrying the standard CD3ζ domain, in the same model. Data available under NDA.

Severe Toxicity

Current therapies carry significant toxicity risk. Severe CRS rates reach 48% in some approved-product trials (ELIANA), and CRS remains a boxed warning across the class.

Calibrated Signaling

26 ITAM variants enable precise tuning of T cell activation. Signal intensity can be matched to clinical context, controlling activation at its source, a mechanism-based route to lower CRS risk that add-on kill switches cannot provide.

Solid Tumor Barrier

CAR-T efficacy in solid tumors remains limited, with a pooled objective response rate of approximately 9% across solid tumor clinical trials.

Low-Antigen Sensitivity

In vitro, ITAM-optimized CAR-T cells showed significantly improved cytotoxicity against low-antigen-expressing targets. Low antigen density is a defining barrier in solid tumors. Preclinical GD2 glioblastoma and HER2 PDX breast cancer programs are advancing. Data available under NDA.

A New Framework for CAR‑T Engineering

NanoKar’s platform was developed in the laboratory of Dr. Matthew Bettini at the University of Utah Department of Pathology, with collaborators in pharmacology, biophysics, and cancer biology. The technology is exclusively licensed to NanoKar Therapeutics. Manuscript under revision (2026). Available to partners under NDA.

The Last Unengineered Domain

Every approved CAR-T uses the same CD3ζ ITAM configuration. NanoKar engineers that configuration across 26 variants, holding the targeting domain, co-stimulatory element, and manufacturing process constant, and shifting the activation signal toward memory formation rather than exhaustion.

CD3 zeta ITAM engineering and resulting T cell fate Three panels. Left, a standard CAR with three identical CD3 zeta ITAMs. Center, the NanoKar version with the same targeting domain and co-stimulatory element but engineered ITAMs. Right, signal strength determining whether the T cell moves toward exhaustion or memory formation. STANDARD CAR Antigen scFv MEMBRANE Co-stim CD3ζ ITAM 1 ITAM 2 ITAM 3 One fixed sequence Identical in every FDA-approved CAR-T NANOKAR ITAM TUNING Antigen scFv unchanged MEMBRANE Co-stim unchanged CD3ζ engineered ITAM 1 ITAM 2 ITAM 3 active tuned inactivated 26 engineered variants Encoded at the DNA level. No manufacturing change. T CELL FATE Signal strength high calibrated Exhaustion PD-1, Tim-3, Lag-3 Short-lived response Memory formation Reduced exhaustion markers Durable tumor control Low-antigen sensitivity Tuned at the source Activation is set by the construct, not corrected downstream. Schematic. Not to scale. Preclinical data available to partners under NDA.

Data generated with ex vivo engineered CAR-T, the format every approved product uses.

Discovery

CARs as Mechanosensors

Demonstrated for the first time that chimeric antigen receptors form catch bonds with antigen, functioning as mechanosensors analogous to T cell receptors. 26 unique predicted signaling profiles with distinct force, bond lifetime, and activation characteristics.

Mechanism

Tunable Signal Strength

Phosphoproteomic analysis (14,000+ unique phosphopeptides) revealed that specific ITAM sequences alter downstream signaling cascades, cytoskeletal dynamics, and metabolic programming. Lower signal intensity correlates with enhanced memory formation.

Efficacy

Xenograft Results

The lead ζ-ITAM construct demonstrates significantly improved tumor control versus the same CAR carrying the standard CD3ζ domain in CD19+ hematological models, with 100% survival across five consecutive weekly tumor re-challenges in a CD19 xenograft B-ALL model. Sustained cytokine production was observed at 29 days post-treatment.

Sensitivity

Low-Antigen Targeting

The leading ζ-ITAM-optimized CAR-T cells demonstrated significantly improved cytotoxicity against low-antigen-expressing targets in vitro.

Intellectual Property: Patent pending. Non-provisional application filed 2025, provisional application filed 2026.
License: Exclusive worldwide license from the University of Utah. Transfers to a successor entity on change of control.

A Platform That Enhances Existing Programs

The technology integrates into any CAR architecture without altering targeting domains, co-stimulatory elements, or manufacturing processes.

Standard CAR‑TNext-Gen ApproachesNanoKar ITAM Optimization
LayerEndogenous CD3ζ signalingExtracellular & structural modificationsIntracellular signaling domain
ExamplesAxi-cel, Tisa-cel, Liso-celArmored CARs, logic gates, allogeneic platforms26 tunable ITAM combinations
Toxicity and PersistenceSevere CRS up to 48% in some approved-product trials (ELIANA); persistence limited by native signalingUp to 100% grade 3+ SAEs in a recent Phase 1; add-on safety switches and co-stimulatory editsBoth tuned at the activation signal source, not managed downstream
ManufacturingBaselineOften requires new vectors, processes, or cell sourcesCompatible with existing workflows. Encoded at the DNA construct level
CompatibilityAutologous T cells onlyPlatform-specific (often single cell type)Any CAR Construct: T cell, NK cell, Macrophage, TCR, BCR and more
DeliveryEx vivo viral transductionPlatform-specific delivery vehiclesDelivery-agnostic. Encoded in the construct, portable across ex vivo and in vivo
RegulatoryEstablished IND pathwayOften requires new IND categoryFits within existing IND frameworks. Positioned for FDA Platform Technology Designation
Competitive Landscape

Orthogonal & Complementary

Nearly every next-generation approach modifies the targeting, structural, or co-stimulatory layer. The intracellular signaling layer has gone unchanged since the first approval. NanoKar works on that fourth layer, so it combines with these approaches rather than replacing them.

Where NanoKar operates within the CAR construct Four engineering layers of a CAR construct. The targeting, structural, and co-stimulatory layers are modified by existing next-generation approaches and owned by the partner program. The intracellular signaling layer, unchanged since the first approval, is where NanoKar operates. CONSTRUCT LAYER WHAT THE FIELD IS DOING OWNED BY Targeting scFv, binder affinity Novel antigens, bispecifics, logic gates Your program Structural Hinge, transmembrane Armored CARs, checkpoint knockouts, gene editing Your program Co-stimulatory CD28, 4-1BB and successors Next-gen co-stim domains, epigenetic programs Your program Intracellular signaling CD3ζ ITAMs Unchanged since the first approval NanoKar Encoded in the construct. Travels with autologous, allogeneic, and in vivo delivery. No overlap. No redesign. No manufacturing change.
Regulatory Pathway

FDA Platform Technology Designation

NanoKar’s platform is positioned to leverage the FDA’s Platform Technology Designation program. Approval of a first ITAM-optimized product could streamline the regulatory path for all subsequent programs built on the same platform.

Where NanoKar Fits Your Pipeline

ITAM optimization creates value differently depending on the program it enters. Four of the most direct fits:

Established CAR‑T

Extend a Maturing Asset

For an approved or clinical CAR-T franchise, ITAM optimization adds a persistence and toxicity differentiator at the construct level, with no change to your targeting domain or manufacturing.

Allogeneic & Solid Tumor

Close the Persistence Gap

Persistence and low-antigen sensitivity are the recurring failure points. ITAM optimization targets both at the signal source and combines with armored, logic-gated, or gene-edited designs.

In Vivo CAR‑T

Optimize the Construct You Deliver

Your delivery stack still carries a CD3ζ construct no one has optimized. ITAM tuning improves what the cell does once engineered, independent of how it is delivered, and every delivery platform acquired to date carries an unoptimized construct.

Autoimmune

Tune Potency Down, Not Just Up

Autoimmune CAR-T needs a controlled immune reset, not maximum activation, in patients who are not facing a terminal diagnosis. Our 26-variant library spans attenuated as well as enhanced signaling, which makes calibrated potency testable. We have not run autoimmune models. Our data is autologous oncology preclinical.

Full in vivo dataset, phosphoproteomics, and construct-level detail are available under NDA. Partners can evaluate lead constructs in their own models under MTA.

Download Company Overview (PDF)

Pipeline

NanoKar is at the preclinical stage with IND-enabling studies planned.

TargetIndicationProgressStage
CD19B-Cell Malignancies (B-ALL, Lymphoma)
Preclinical Validation
HER2Breast Cancer (Solid Tumor)
Preclinical Validation
GD2Glioblastoma (Solid Tumor)
Preclinical Validation
Nectin4Bladder Cancer
Pending
EGFRvIIIGlioblastoma (Solid Tumor)
Pending
B7-H3Ovarian Cancer
Pending
BCMAMultiple Myeloma
Pending

Research

Under Revision

Selective CD3ζ ITAM Engineering of Chimeric Antigen Receptors Tunes Catch Bond Dynamics and Function

Echelibe H, Kolawole EM, Majumdar S, Lee W, Spainhower K, Liu B, Jensen P, Bettini M, Golkowski M, Evavold BD, Bettini ML. Manuscript under revision (2026). Available to partners under NDA.

Our Team

Craig Mosman
Craig Mosman, J.D.
Chief Executive Officer
Leading NanoKar’s operations and IND-enabling program planning. Co-founded Seek Labs, where he led business development for nearly a decade. Former President of Kirkland Biotechnologies, investing in and commercializing early-stage biotech companies. J.D. with international business development experience across six continents.
Matt Bettini, Ph.D.
Matt Bettini, Ph.D.
Founder & Chief Scientific Officer
Inventor of NanoKar’s ITAM optimization platform and named inventor on the company’s foundational patent application. Senior author on the manuscript currently under revision. Professor at the University of Utah Department of Pathology, with 15 years of expertise in immune tolerance, T cell engineering, and CAR-T mechanobiology. Ph.D. from Emory University with postdoctoral training at St. Jude Children’s Research Hospital.
Ross Eldridge
Ross Eldridge
Founder & Board Member
Seasoned healthcare investor across private credit and private equity. Two decades of experience and $35B+ in career transaction volume, with board roles across portfolio companies. Co-founded NanoKar to bring institutional-grade capital discipline and governance to early-stage therapeutic development.

Scientific Advisory Board

NanoKar’s advisors are affiliated with Huntsman Cancer Institute and the University of Utah.

Daniel Couriel, MD, MS, MBA
Scientific Advisor
Medical Director, Huntsman Cancer Institute Center for Cellular Therapy & Regenerative Medicine. Endowed Chair in Hematology at the University of Utah. Board member for ASTCT and FACT.
Alana Welm, Ph.D.
Scientific Advisor
Senior Director of Basic Science at Huntsman Cancer Institute. 20 years of experience with preclinical cancer therapeutics in mouse and patient-derived models.
Jens Lohr, MD, Ph.D.
Scientific Advisor
Director of CellReGen and Director of Immunotherapy Research at the University of Utah. Faculty at Huntsman Cancer Institute. Translational focus on multiple myeloma and cellular therapies. M.D./Ph.D. from Heidelberg, hematology/oncology fellowship at Dana-Farber/Harvard.

Latest Announcements

Press Release June 9, 2026

NanoKar Therapeutics Accepted into Innosphere Ventures Accelerator Program

NanoKar Therapeutics has been accepted into the Innosphere Ventures accelerator program in Fort Collins, Colorado. The program provides mentorship, investor access, and business development support as NanoKar advances its ITAM optimization platform for CAR-T cell therapy toward strategic partnerships.

Read the full release
Press Release June 2, 2026

NanoKar Therapeutics Receives Funding From the University of Utah Launchpad Seed Fund to Advance Next-Generation CAR‑T Cell Therapy Platform

NanoKar Therapeutics has been awarded funding from the University of Utah Launchpad Seed Fund to advance its ITAM optimization platform for CAR-T cell therapy. The capital will support translational validation data, including CAR-T persistence and activity in solid tumor models, and help prepare the platform for evaluation by potential development partners.

Read the full release
Press Release May 28, 2026

NanoKar Therapeutics Announces Formal Appointment of Craig Mosman as Chief Executive Officer

NanoKar Therapeutics has formally appointed Craig Mosman, J.D., as Chief Executive Officer. Mosman will lead the company’s partnership strategy and translational data priorities as it advances the ITAM optimization platform toward partner-ready commercialization.

Read the full release
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Partner with NanoKar

NanoKar is advancing discussions with strategic partners across the cell therapy landscape. If our platform aligns with your programs or investment focus, we’d welcome a conversation.

Craig Mosman, Chief Executive Officer
craig@nanokartherapeutics.com
Altitude Lab
Attn: NanoKar Therapeutics
48 South Rio Grande Street
Salt Lake City, UT 84101
Forward-Looking Statements

This website may contain forward-looking statements regarding NanoKar Therapeutics, Inc., including statements about the company’s research and development programs, the potential of its ITAM optimization platform, anticipated preclinical and clinical milestones, intellectual property, and plans for partnerships, financing, and commercialization. These statements are based on current expectations and assumptions and are subject to risks and uncertainties, including but not limited to risks associated with preclinical and clinical research, the timing and outcome of regulatory submissions and approvals, the success of clinical trials, manufacturing and supply, intellectual property protection and freedom to operate, competitive products and technologies, and the availability of financing on acceptable terms. Actual results may differ materially from those expressed or implied. NanoKar Therapeutics undertakes no obligation to update any forward-looking statement except as required by law. Nothing on this website constitutes an offer to sell or a solicitation of an offer to buy any securities, and no securities of NanoKar Therapeutics may be offered or sold in any jurisdiction in which such offer or sale would be unlawful.