NDI-101150 

NDI-101150 is an orally active, potent and selective hematopoietic progenitor cell kinase 1 (HPK1) inhibitor with an IC₅₀ of 0.7 nM. NDI-101150 blocks HPK1-mediated negative regulation of immune receptor signaling, inhibits immunosuppression of T cell activation, enhances antigen-specific antibody production and augments B-cell activation. NDI-101150 inhibits tumor growth in syngeneic tumor models, establishes durable antitumor immune memory, and synergizes with anti-PD1 to enhance exhausted T cell activity and drive tumor regressions. NDI-101150 can be used for the research of cancer, such as breast cancer and colon cancer^[1][2].

NDI-101150 potently and selectively inhibits HPK1 in a cell-free biochemical assay with an IC₅₀ of 0.7 nM, and exhibits high fold-selectivity over closely related MAP4K family kinases and immune cell signaling kinases^[1].
NDI-101150 potently inhibits HPK1 in a cell-based assay with an IC₅₀ of 41 nM^[1].
NDI-101150 (1-10000 nM) reverses TGF-β-, PGE₂, T_REG, Adenosine (HY-B0228)-induced immunosuppression of human T cells, restoring IFN-γ, IL-2 production to naive T cell levels^[1].
NDI-101150 (0.003-1.0 μM) induces dose-dependent increases in IFN-γ, TNF-α, and GM-CSF production in human mixed lymphocyte reactions, with responses surpassing naive T cell levels^[1].
NDI-101150 reinvigorates exhausted human T cells, restoring IL-2 secretion after a 10-day stimulation/rest exhaustion protocol^[1].
NDI-101150 is a highly potent and selective cell-free inhibitor of HPK1 kinase activity, with an IC₅₀ of 0.7 nM, and exhibits exceptional selectivity over other MAP4K family members and critical immune cell kinases^[2].
NDI-101150 dose-dependently inhibits SLP-76 phosphorylation in anti-CD3-stimulated human Jurkat T cells, with an IC₅₀ of 41 nM^[2].
NDI-101150 dose-dependently inhibits SLP-76 phosphorylation in anti-CD3-stimulated human CD4⁺ and CD8⁺ T cells (IC₅₀ = 21 nM and 20 nM, respectively) without reducing cell viability^[2].
NDI-101150 dose-dependently inhibits BLNK phosphorylation in anti-IgM-stimulated human B cells, with an IC₅₀ of 48 nM^[2].
NDI-101150 (0.001-1.0 μM; 72-96 h) dose-dependently enhances anti-CD3/CD28-induced cytokine secretion and proliferation in human primary CD4⁺ and CD8⁺ T cells, with EC₅₀ values ranging from 11-17 nM for cytokines, and does not reduce cell viability^[2].
NDI-101150 (0.0015-3.3 μM) dose-dependently enhances IFN-γ production in human mixed lymphocyte reactions^[2].
NDI-101150 (0.03-3.0 μM) dose-dependently enhances anti-IgM-induced CD19⁺ B-cell activation, IgG secretion, and proliferation^[2].
NDI-101150 (1-10000 nM; 24-48 h) dose-dependently restores and enhances T-cell activation in human primary T cells suppressed by TGF-β, PGE₂, or Adenosine, with cytokine secretion exceeding naïve T-cell levels at higher concentrations^[2].
NDI-101150 (0.003-1.0 μM) dose-dependently reactivates exhausted human T cells in MLRs, inducing proliferation and cytokine secretion, and shows synergistic effects when combined with anti-PD-1^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

NDI-101150 (75 mg/kg; p.o.; once daily for 17 days) induces ~70% tumor growth inhibition, enhances systemic and tumor-localized immune activation, and generates durable immune memory in female BALB/c mice with syngeneic EMT-6 tumors^[2].
NDI-101150 (75-150 mg/kg; p.o.; once daily for 12-20 days) induces ~40% tumor growth inhibition and enhances proinflammatory cytokine and antibody production in female BALB/c mice with anti-PD-1-resistant syngeneic CT-26 and B16F10 tumors^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

486.54

C₂₇H₂₇FN₆O₂

2628486-22-4

O=C1NCC2=C(C3=CN=C4N3C=CC(F)=C4)C=CC(NC5=CC=C([C@@]6([H])COCC6)C(CN(C)C)=N5)=C21

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Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Ciccone D, et al. NDI-101150 is a potent and highly selective HPK1 inhibitor that both synergizes with and differentiates from anti-PD1 immune checkpoint blockade[C]//Cancer Research. 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA: AMER ASSOC CANCER RESEARCH, 2024, 84(6).

  [2]. Ciccone DN, et al. Highly selective HPK1 inhibitor NDI-101150 mediates immune cell activation and robust antitumor responses, distinct from immune checkpoint blockade. J Immunother Cancer. 2025;13(7):e012064. Published 2025 Jul 30.  [Content Brief]