Company: HURA
Filing Date: 2025-05-23
Form Type: 424B3
Source: 0001193125-25-125499
Chunk: 426

Company: TuHURA Biosciences, Inc./NV
Filing Date: 2025-05-23
Form: 424B3
Chunk 426
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1, followed by anti-PD-1/anti-CTLA-4 therapy. All seven patients exhibited primary resistance to checkpoint inhibitor therapy progressing on average 3.3 months while receiving CPI therapy. These seven patients are
graphically presented below:

This data demonstrating the potential for IFx-2.0 to overcome
primary resistance to anti-PD(L)-1 therapy and formed the clinical rationale for examining IFx-2.0 as adjunctive therapy with
Keytruda(anti-PD-1) in first line therapy among checkpoint inhibitor naïve patients with advanced or
metastatic Merkel cell carcinoma. Unlike the phase 1b where IFx-2.0 was administered after patients progressing on anti-PD(L)-1
therapy, we believe IFx-2.0 could potentially provide a higher response rate to Keytruda when administered prior to patients progressing failing
Keytruda.

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The remaining seven (7) patients received multiple checkpoint inhibitor therapy
including anti-CTLA-4/anti-PD-1 therapy and/or investigational agent(s) and or chemotherapy as 2 or 3 line therapy prior to treatment with IFx-2.0. This patient population is not
representative of patients to be enrolled in the phase 3 trial.

Importantly, IFx-2.0 is not an
intratumoral therapy like oncolytic viral therapies whose anti-tumor activity is limited to accessible, injected lesions in limited stages of cancer. In contrast, IFx-2.0’s mechanism of action is to prime
and activate an innate immune response in injected lesions leading to a systemic anti-tumor response. The Company chose to examine IFx-2.0 in cutaneous malignancies because human skin has a high density of DCs
which are very efficient in presenting foreign antigens to immune cells. Local injection of IFx-2.0 into cutaneous lesion(s) has resulted in immune cell infiltration, and in the context of MHCI and MHCII,
tumor neoepitope presentation to naïve B and T cells followed by activation of tumor specific B and T cells. The immune response has not been localized to just injected lesions but rather systemic as demonstrated by production of Emm55 (pDNA
encoded bacterial protein expressed on the surface of the tumor cell) and tumor specific IgM and IgG antibodies in the plasma of patients post IFx-2.0 administration.

Patients Merkel cell carcinoma-03 and Merkel cell carcinoma-05
below