Science & Technology

The MILs™ platform has the power and flexibility to improve cell therapies across the medical landscape, creating better, more durable clinical responses in patients.

We intend to explore the vast possibilities for leveraging the differentiating features of MILs to create a broad pipeline of next-generation cell therapies based on our unique and proprietary process of activating and expanding memory T cells from the bone marrow.

WindMIL is open to partnerships and collaborations to further explore use of unmodified MILs and genetically-modified MILs. Potential partners and collaborators are invited to contact WindMIL at

MILs Platform infographic


Power and flexibility of the MILs Platform

MILs have the potential to be used in both unmodified and gene-modified forms, creating next-generation cell therapies that are well-suited to address the diversity of treatment approaches required by today’s cancer patients.

Unmodified MILs™

  • Naturally tumor-specific, unmodified MILs recognize a broad spectrum of cancer antigens, are superior tumor cell killers and highly persistent
  • Unmodified MILs (alone and in combination) are being explored to treat hematologic malignancies and solid tumors
  • Our two lead clinical programs are exploring use of MILs as novel autologous cell therapies to treat high-risk multiple myeloma and non-small cell lung cancer
    • High-risk multiple myeloma: Fully-enrolled, randomized, multi-center Phase 2 study (two-year data readout in 2H 2020)
    • NSCLC (PD-1 relapsed/refractory): Open label, single-arm, multi-center Phase 2a study of MILs in combination with an anti-PD-1 (initiating 2H 2019)
  • WindMIL is quickly advancing additional MILs programs in both hematologic and solid tumors
    • WindMIL plans to launch additional studies in early 2020 in other solid tumor indications
  • WindMIL is open to collaborations to further explore use of unmodified MILs

Genetically Modified MILs

  • CAR-MILs™ – Current chimeric antigen receptor T-cell (CAR T) therapies face three challenges: antigen escape variants, suboptimal trafficking into the tumor microenvironment and lack of persistence. MILs are an ideal backbone for better CAR T therapies due to their natural tumor specificity and memory T-cell phenotype, which is a less ‘exhausted’ phenotype than the effector T cells found in the peripheral blood (the source of T cells for current CAR therapies). Specifically, MILs:
    • Retain non-CAR-based tumor specificity through the native TCR – CAR T therapy has led to meaningful remissions for cancer patients. But advances have come by targeting only a single antigen expressed on a tumor cell. Targeting just one antigen allows the cancer to ultimately develop ways to evade the immune system (via the formation of antigen-escape variants). A key MILs feature is their polyclonal makeup and natural ability to recognize and kill numerous tumor cell variants via their native T-cell receptor (TCR) even after transduction and CAR engagement.
    • Home to both the tumor site via increased CXCR4 expression – Expression of SDF-1 in the stroma of solid tumors acts as a beacon for MILs, guiding the therapy to the tumor site where it can engage and kill tumor cells.
    • At lower effector to target ratios, CAR-MILs are more effective than CAR-PBLs – WindMIL has demonstrated in vitro that the memory phenotype of CAR-MILs enhances the killing ability of MILs as demonstrated in cellular assays.
    • Persist over the long-term – the memory phenotype of MILs is also responsible for their persistence in vivo. MILs are detectable up to eight years post-infusion and also display superior efficacy over repeated challenge.
  • X-MILs – There is also great potential for developing cell therapies based on MILs with other novel genetic modifications. Such modifications could act as a payload leveraging the inherent tumor specificity of MILs. Alternatively, genetic modifications could include changes to boost cell-killing activity, or modifications to counter tumor cells’ efforts to evade the immune system.