MiNK Therapeutics Inc (INKT)

[dia76ca]

Mink SITC 2022 posters are full of very exciting data! Here are some highlights.

1.Allogeneic unmodified iNKTs (agenT-797) show reductions in target and non-target lesions or disease stabilization in patients with solid
tumor cancers when administered alone [27%] and in combination with pembrolizumab (KEYTRUDA®) or nivolumab (OPDIVO®) [66%].
Phase 1 data show early signals of activity with disease stabilization in patients refractory to standard of care and those
who have progressed on KEYTRUDA or OPDIVO.
agenT-797 preferentially kills tumor-promoting M2 macrophages while preserving pro-inflammatory M1 macrophages
associated with anti-tumor responses.
agenT-797 can be dosed up to 1000x106
cells without lymphodepletion showing no signs of neurotoxicity and cytokine release syndrome (CRS grade ≥ 3).

2.Allo-iNKTs show signals of durable disease stabilization and modulation of M-spike protein seen in heavily pre-treated r/r multiple myeloma patients (2/8) after ≥6 prior lines of therapy.

3. agenT-797 shows 70% survival in severe viral ARDS compared to site reference controls (~10%); potential for a variant agnostic approach
to infections. In Phase 1/2 study, agenT-797 shows survival of 70% in mechanically ventilated patients compared to ~10% in a comparative case control population.

4. Increased 90-day survival in a subgroup of patients on respiratory bypass (ECMO) of 75% compared to 30% in a
comparative cohort with median survival of 119.5 vs 47 days.
agenT-797 demonstrates a favorable safety profile. Only 1 grade ≥3 treatment related adverse event and no CRS was
observed. agenT-797 treatment was associated with a reduction in secondary infections, including reduced incidence of pneumonia at
the highest dose level, a driver of ICU mortality.

5. MiNK’s FAP-CAR-iNKT therapeutic candidate, MiNK-215, demonstrates robust efficacy in non small cell lung cancer (NSCLC) preclinical
models, promoting curative responses, eliminating tumor burden in the lungs, and enhancing tumor specific CD8+ T cell infiltration
through tumor stroma.
FAP-CAR-iNKT demonstrates a drastic increase of CD8+ T cells infiltrating the tumor and significantly increased tumor
killing compared to T cells in murine models.
MiNK-215 shows robust preclinical efficacy towards tumor expressing FAP (FAP+ cancer model), underscoring potential to
target FAP+ tumors.

6. MiNK-413 is a differentiated allogeneic IL-15-armored-BCMA-CAR-iNKT therapeutic candidate, a next generation approach designed to
overcome the limitations of current autologous cell therapies.
MiNK-413 demonstrates superior tumor clearance in a systemic multiple myeloma models, compared to control BCMA-CAR.
Armoring MiNK-413 with soluble IL-15 enables prolonged persistence, which may translate to increased durability in patients.
MiNK-413 has the potential to target a broader population of patients with multiple myeloma.

7. MiNK’s proprietary CARDIS platform enables high-throughput rapid selection and optimization of functional CARs, like
MiNK-413 (IL-15-armored-BCMA-CAR-iNKT) and MiNK-215 (FAP-CAR-iNKT).

Allo-iNKTs (agenT-797) reinvigorate partially exhausted T cells and improve effector functions within the tumor microenvironment; critical
mechanisms in rescuing PD-1 refractory tumors.
In addition to their direct anti-tumor activity, allogeneic iNKT cells (agenT-797) improve immune effector function of immune
cells in the tumor microenvironment.
agenT-797 restores the cytotoxic capacity, activation, and cytokine production of partially exhausted T cells. agenT-797 preferentially kills tumor-promoting M2 macrophages while preserving pro-inflammatory M1 macrophages associated with anti-tumor responses.
agenT-797 activates dendritic cells, which can promote activation of T cells through enhanced antigen presentation.

The full poster presentations can be accessed on the publication section of MiNK’s website at https://minktherapeutics.com/publications/.