P1, N=2, Terminated, University of Oxford | N=54 --> 2 | Not yet recruiting --> Terminated; Delayed due to COVID19. Study drug expired before could be used.

P1, N=24, Recruiting, Fox Chase Cancer Center | Not yet recruiting --> Recruiting

P2, N=120, Not yet recruiting, Incyte Corporation

P1, N=32, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Phase classification: P1b --> P1 | Trial completion date: Jan 2024 --> Jan 2025 | Trial primary completion date: Jan 2024 --> Jan 2025

P1, N=10, Completed, Blueprint Medicines Corporation | Recruiting --> Completed | N=20 --> 10 | Trial completion date: Dec 2023 --> Apr 2024 | Trial primary completion date: Nov 2023 --> Mar 2024

P2, N=100, Recruiting, GB002, Inc., a wholly owned subsidiary of Gossamer Bio, Inc. | Trial completion date: Jul 2025 --> Dec 2027 | Trial primary completion date: Jul 2025 --> Dec 2027

P3, N=40, Active, not recruiting, Daiichi Sankyo Co., Ltd. | Trial completion date: Mar 2024 --> Feb 2026

P3, N=90, Active, not recruiting, Abbisko Therapeutics Co, Ltd | Recruiting --> Active, not recruiting

P=N/A, N=6, Active, not recruiting, Daiichi Sankyo Co., Ltd. | Phase classification: P1/2 --> P=N/A | Trial completion date: Mar 2024 --> Mar 2025

More importantly, C19 combined with PD-1 mAb could induce durable antitumor immune memory, effectively overcoming the recurrence of CRC. Taken together, our findings suggest that C19 is a promising therapeutic option for sensitizing CRC to anti-PD-1 therapy.

P3, N=120, Active, not recruiting, Deciphera Pharmaceuticals LLC | Trial primary completion date: Mar 2024 --> Aug 2023

Furthermore, we evaluated the sensitivity of these mutants to three FDA-approved tyrosine kinase inhibitors: imatinib, dasatinib, and avapritinib, which effectively suppressed the constitutive activity of the mutant receptors. Interestingly, K385M was reported in a few cases of brain tumors but not in MGNT. Our results provide valuable insights into the molecular mechanism underlying the activation of PDGFRα by the K385I/L mutations, highlighting their potential as actionable targets in the treatment of myxoid glioneuronal tumors.

Oxygen-glucose deprivation causes an increase in NR4A1 mRNA in astrocytes as well as its nuclear to cytoplasmic transfer. Furthermore, reoxygenation enhances NR4A1 transcription and promotes its nuclear translocation.

P1, N=34, Recruiting, H. Lee Moffitt Cancer Center and Research Institute

P1/2, N=38, Not yet recruiting, OHSU Knight Cancer Institute

P1, N=36, Not yet recruiting, Abbisko Therapeutics Co, Ltd

P2, N=25, Recruiting, University of Washington | Trial completion date: Nov 2024 --> Nov 2026 | Trial primary completion date: Nov 2024 --> Nov 2026

P1/2, N=88, Active, not recruiting, Vanderbilt-Ingram Cancer Center | Trial primary completion date: Jul 2024 --> Feb 2024

P2, N=50, Recruiting, Children's Hospital of Soochow University

P1/2, N=36, Recruiting, Chipscreen Biosciences, Ltd. | Phase classification: P1b/2 --> P1/2

P2, N=4, Completed, University of Michigan Rogel Cancer Center | Active, not recruiting --> Completed

P1/2, N=43, Active, not recruiting, Gulam Manji | Recruiting --> Active, not recruiting | Phase classification: P2 --> P1/2 | Trial completion date: Mar 2024 --> Jun 2024

P1/2, N=160, Not yet recruiting, National Cancer Institute (NCI)

P1/2, N=120, Recruiting, Qurient Co., Ltd. | Phase classification: P1b/2 --> P1/2

RNA-seq further confirms the enhanced immune cell function. Consequently, P@ZIF/M1-KTP has great potential as a novel adoptive cellular therapeutic strategy for tumors.

In vivo, PXB17 significantly halted CRC growth, with a stronger effect than PLX3397. In particular, PXB17 potently enhanced therapeutic activity of PD-1 mAb in CT-26 (MSS) model and prevented tumor recurrence in MC-38 (MSI-H) model by promoting formation of long-term memory immunity. Our study opens a new avenue for CSF1R in tumor innate and adaptive anti-tumor immunomodulatory activity and suggests that PXB17 is a promising immunotherapy molecule for enhancing the efficacy of PD-1 mAb or reducing tumor recurrence of CRC.

Finally, pacritinib suppressed KSHV viral IL-6-induced human IL-6 and IL-10 production in peripheral blood mononuclear cells, which may model an important step in KSHV-MCD pathogenesis. These results suggest that pacritinib warrants testing for the treatment of KSHV-MCD and PEL.

P1/2, N=200, Recruiting, Nerviano Medical Sciences | N=140 --> 200 | Trial completion date: Sep 2023 --> Feb 2026 | Trial primary completion date: Sep 2023 --> Dec 2025

P2, N=5, Completed, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins | Active, not recruiting --> Completed | Trial completion date: Sep 2025 --> Feb 2024

P3, N=20, Not yet recruiting, Incyte Biosciences Japan GK

P2, N=56, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting

Vorolanib plus nivolumab had a manageable safety profile and may have clinical benefits in various thoracic malignancies. The disease control rate in thymic malignancies warrants further assessment.

Combining ADCT-602 + pacritinib was beneficial in ADCT-602-resistant cells. Chidamide increased CD22 expression on B-cell tumor surfaces, increasing ADCT-602 activity. These data support clinical testing of ADCT-602 in R/R B-ALL (NCT03698552) and CD22-positive hematological cancers.

P1, N=60, Completed, CTI BioPharma | Active, not recruiting --> Completed

P2, N=6, Active, not recruiting, Medical College of Wisconsin | Recruiting --> Active, not recruiting

Treatment by PLX3397 in combination with paclitaxel significantly inhibited the growth of ovarian cancer both in vitro and in vivo. Blockade of CSF-1R altered the macrophage phenotype and reprogrammed the immunosuppressive cell population in the tumor microenvironment.

P1, N=33, Completed, M.D. Anderson Cancer Center | Active, not recruiting --> Completed

No abstract available

P1, N=12, Completed, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins | Active, not recruiting --> Completed

Our results demonstrate that pexidartinib, through the inhibition of FLT3 signaling, has a deleterious effect on DC differentiation, which may explain the limited antitumor clinical activity observed in this study. This work suggests that inhibition of FLT3 should be considered when combining TKIs with immune checkpoint inhibitors.

P2, N=135, Recruiting, Syndax Pharmaceuticals | Not yet recruiting --> Recruiting

P1, N=24, Not yet recruiting, Fox Chase Cancer Center