Drug-enhanced Cell Therapy Programs
Adoptive Cell Therapy
Nurix is pioneering applying targeted protein modulation to adoptive cell therapy. Our lead cell therapy program applies a CBL-B inhibitor, NX-0255, to a cancer patient’s T cells outside the body (ex vivo) to enhance their tumor-killing ability when returned to the patient as an autologous cell therapy. Inhibiting CBL-B has several beneficial effects that enhance adoptive T cell therapy, including stimulation of IL-2 secretion, increased T cell proliferation, reduced T cell exhaustion, and a skewing of the phenotype of the T-cells for improved clinical outcomes.
| Drug Candidate | Target (Delivery) | Therapeutic Area | Discovery | IND enabling | Phase 1 | Phase 2 | Phase 3 | |
|---|---|---|---|---|---|---|---|---|
| Clinical Pipeline | ||||||||
| NX-2127 Degrader | BTK + IMiD Activity (Oral) | B-cell malignancies |
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| NX-5948 Degrader | BTK (Oral) | B-cell malignancies and autoimmune disease |
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| NX-1607 Inhibitor | CBL-B (Oral) | Immuno-oncology |
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| DeTIL-0255 Cell Therapy | Adoptive cell therapy with ex vivo CBL-B inhibition | Gynecologic malignancies |
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| Drug Candidate | Target (Delivery) | Therapeutic Area | Discovery | IND enabling | Phase 1 | Phase 2 | Phase 3 | |
| Discovery Pipeline | ||||||||
| Wholly Owned | Multiple targets* | Undisclosed |
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| Gilead Sciences | 5 targets | Undisclosed |
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| Sanofi | 5 targets | Undisclosed |
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| Candidate / Target | Phase |
|---|---|
| Clinical Pipeline | NX-2127 Degrader BTK + IMiD Activity (Oral) | Phase 1 |
| NX-5948 Degrader BTK (Oral) | Phase 1 |
| NX-1607 Inhibitor CBL-B (Oral) | Phase 1 |
| DeTIL-0255 Cell Therapy Adoptive cell therapy with ex vivo CBL-B inhibition | Phase 1 |
| Discovery Pipeline | Wholly Owned Multiple targets* | Discovery |
| Gilead Sciences 5 targets | Discovery |
| Sanofi 5 targets | Discovery |
DeTIL-0255 (drug-enhanced tumor-infiltrating lymphocytes for solid tumors)
DeTIL-0255 is a cellular therapy that incorporates our proprietary small molecule CBL-B inhibitor NX-0255 in the cell expansion process of tumor infiltrating lymphocytes (TIL). We call this drug-enhanced TIL, or DeTIL. While DeTIL-0255 incorporates a CBL-B inhibitor, we are also exploring combining other targeted agents, such as its proprietary protein degraders, to enhance T cell expansion and phenotypes.
We are planning to first develop DeTIL-0255 in multiple solid tumors as a monotherapy and later to combine it with our proprietary oral CBL-B inhibitor, NX-1607. A Phase 1 clinical trial of DeTIL-0255 in gynecological malignancies is ongoing.
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