Table 2.
Overview of completed clinical trials testing telaglenastat (CB-839) in various cancer patients.
| Cancer Type | Treatment | Outcome | Reference |
|---|---|---|---|
| Triple-negative breast cancer (TNBC) | In combination with paclitaxel (chemotherapeutic agent targeting microtubules) | In heavily pretreated patients with previous taxane exposure, the treatment demonstrated clinical activity and was well tolerated. | [172] |
| Clear cell renal cell carcinoma (ccRCC), melanoma; non-small-cell lung cancer (NSCLC) | In combination with nivolumab (immunotherapy medication targeting programmed cell death (PD-1) receptor) | CB-839 was well tolerated when combined with nivolumab in melanoma, ccRCC, and NSCLC patients. |
[173] |
| Solid tumors with K-Ras mutation | In combination with palbociclib (kinase inhibitor targeting cyclin-dependent kinases CDK4 and CDK6) | NA | NA |
| Solid tumors | As a single agent and in combination with standard chemotherapy | Acceptable safety profile under continuous CB-839 administration. Treatment resulted in glutaminase inhibition and clinical activity. | [174] |
| Hematological tumors | As a single agent or in combination with pomalidomide (immunomodulatory agent), dexamethasone (glucocorticoid), or pomalidomide and dexamethasone | CB-839 administration was well tolerated and resulted in GLS inhibition in blood platelets and in tumors. Observed reductions in marrow and peripheral blast counts suggested clinical relevance. | [175] |
| Renal cell carcinoma (RCC) | In combination with cabozantinib (tyrosine kinase inhibitor) | Did not achieve primary endpoint. | [176] |
| ccRCC | In combination with everolimus (mammalian target of rapamycin (mTOR) kinase inhibitor) | In combination with everolimus, CB-839 demonstrated a tolerable safety profile. Modest (3.8 months from 1.9 months) progression-free survival was observed. | [177] |
| Leukemia | CB-839 as a single agent or in combination with azacitidine (chemotherapeutic agent, antimetabolite) | CB-839 was well tolerated in advanced leukemia and resulted in GLS inhibition in platelets and PBMCs. Two patients achieved significant reductions in blast counts. |
[175] |