2. Immunology/Inflammation
  3. Interleukin Related
  4. Nanrilkefusp alfa

Nanrilkefusp alfa  (Synonyms: SO-C101; SOT101)

Cat. No.: HY-P3379

Nanrilkefusp alfa (SO-C101; SOT101) is fusion protein, is a selective and potent agonist fusion protein of IL-15 and IL-15Rα sushi+ domain. Nanrilkefusp alfa inhibits tumor by inducing proliferation and activation of memory CD8+ T cells, natural killer (NK) cells, γ/δ T cells and NKT cells. Nanrilkefusp alfa exhibits excellent anti-metastatic activity against melanoma and suppresses tumor growth in various mouse tumor models.

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Nanrilkefusp alfa Chemical Structure

Nanrilkefusp alfa Chemical Structure

CAS No. : 1416390-27-6

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Description

Nanrilkefusp alfa (SO-C101; SOT101) is fusion protein, is a selective and potent agonist fusion protein of IL-15 and IL-15Rα sushi+ domain. Nanrilkefusp alfa inhibits tumor by inducing proliferation and activation of memory CD8+ T cells, natural killer (NK) cells, γ/δ T cells and NKT cells. Nanrilkefusp alfa exhibits excellent anti-metastatic activity against melanoma and suppresses tumor growth in various mouse tumor models[1][2].

IC50 & Target[1][2]

IL-15

 

IL-15Rα

 

In Vitro

Nanrilkefusp alfa (0.01-10 nM; 7 d) expands and activates NK cell subtypes from human PBMCs in vitro[1].
Nanrilkefusp alfa (1 nM; 20 h) induces cytotoxic and tumor cell-killing activity of human NK cell subtypes[1].
Nanrilkefusp alfa (0.1, 1, and 10 nM; 3 d and 7 d) induces expression of cytotoxic receptors NKp30, DNAM-1 and NKG2D on human NK cells[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo

Nanrilkefusp alfa (2 mg/kg; s.c.; 4 consecutive days over 2 weeks) decreases the rate of tumor development and growth in metastatic kidney cancer Renca mouse model in dependence on natural killer (NK) and CD8+ T cells. And Nanrilkefusp alfa also activates NK and CD8+ T cytotoxicity genes in the TC-1 tumor model[1].
Nanrilkefusp alfa (1 mg/kg; i.p.; 4 consecutive days over 2 weeks) with 12.5 mg/kg anti-PD-1 decreases tumor growth of established TRAMP-C2 tumors and expands the populations of CD8+ T cells and NK cells, but not T regulatory cells (Tregs). And Nanrilkefusp alfa also mediates inhibition of TRAMP-C2 tumor development depending mainly on NK and CD8+ T cells[2].

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

Animal Model: Metastatic kidney cancer Renca mouse model[1]
Dosage: 2 mg/kg
Administration: Subcutaneous injection; for 4 consecutive days over 2 weeks
Result: Decreased the rate of the tumor development.
Decreased the tumor growth of established TC-1 tumors in dependence on NK and CD8+ T cells, but not CD4+ T cells.
Expanded immune cells in tumor, lymph nodes and spleen and activates NK and CD8+ T cytotoxicity genes in TC-1 tumor mouse model.
Animal Model: TRAMP-C2 tumors mouse model[2]
Dosage: 1 mg/kg; with or without 12.5 mg/kg anti-PD-1
Administration: Intraperitoneal injection; for 4 consecutive days over 2 weeks
Result: Prevented tumor development with anti-PD-1 in the majority of TRAMP-C2 mouse and delays tumor growth after re-challenge.
CAS No.
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Keywords:

Nanrilkefusp alfa1416390-27-6SO-C101 SOT101SOT101SOT 101SOT-101Interleukin RelatedILInhibitorinhibitorinhibit

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