Company: MBIO
Filing Date: 2025-04-01
Form Type: 424B3
Source: 0001104659-25-030657
Chunk: 18

Company: MUSTANG BIO, INC.
Filing Date: 2025-04-01
Form: 424B3
Chunk 18
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. This
clinical response was sustained for 7.5 months after the initiation of CAR T-cell therapy; however, the patient’s disease eventually
recurred at four new locations that were distinct and non-adjacent to the original tumors, and biopsy of one of these lesions showed decreased
expression of IL13Rα2.

Results from this COH study have laid the foundation
for three MB-101 studies that are currently enrolling patients and one possible combination study in the future:

| 1. | MB-101 with or without nivolumab and ipilimumab in treating patients with recurrent or refractory glioblastoma (currently enrolling patients; ClinicalTrials.gov Identifier: NCT04003649) sponsored by COH; |

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| 2. | MB-101 in treating patients with recurrent or refractory glioblastoma with a substantial component of leptomeningeal disease (currently enrolling patients; ClinicalTrials.gov Identifier: NCT04661384) sponsored by COH; |

| 3. | MB-101 in treating children with recurrent or refractory IL13Rα2 positive brain tumors (currently enrolling patients; ClinicalTrials.gov Identifier: NCT04510051) sponsored by COH; |

| 4. | MB-101 in combination with the herpes simplex virus type 1 oncolytic virus (MB108) in treating patients with recurrent or refractory glioblastoma or high-grade astrocytoma, as described above. We refer to this combination therapy as MB-109, and we are currently exploring with COH and Nationwide the possibility of conducting a Phase 1 trial with this therapy to treat patients with these poor-prognosis malignant brain tumors. This trial would be an investigator-sponsored single-institution trial under the COH IND and could potentially be initiated in the fourth quarter of 2025 |

MB-108 (HSV-1 oncolytic virus C134)

MB-108 is a next-generation oncolytic herpes simplex
virus (“oHSV”) that is conditionally replication competent; that is, it can replicate in tumor cells, but not in normal cells,
thus killing the tumor cells directly through this process. Replication of C134 in the tumor itself not only kills the infected tumor
cells but causes the tumor cell to act as a factory to produce new virus. These virus particles are released as the tumor cell dies and
can then proceed to