Amulirafusp alfa
Based on 1 Customer Validation
Amulirafusp alfa (IMM-0306) is a fusion protein of CD20 monoclonal antibody (mAb) with the CD47 binding domain of SIRPα, with human CD20 Kd 2.45 nM and human CD47 Kd 4.91 nM. Amulirafusp alfa binds to CD20 and CD47 on B cells, engages FcɣR, blocks CD47-SIRPα interaction, activates macrophages, NK cells, and complement cascade, mediates phagocytosis and cytotoxicity, inhibits apoptosis of Jurkat-CSR cells, reverses IL-16 tumor-promoting effects, and binds human/cynomolgus CD47 but not mouse/rat CD47. Amulirafusp alfa can be used for the research of hematological malignancies, relapsed or refractory CD20-positive B-cell non-Hodgkin’s lymphoma, relapsed or refractory B-cell non-Hodgkin lymphoma, and activated B-cell-like diffuse large B-cell lymphoma.
For research use only. We do not sell to patients.
- Purity: 99.89%
- CAS No.: 2850355-94-9
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Human IgG1 kappa
Human
MS4A1/CD47[1]
Amulirafusp alfa (0.0001-10000 nM) binds with high affinity to CD47 on Jurkat cells (EC50 = 16.83 nM), CD20 on Raji-CD47KO cells (EC50 = 18.92 nM), and both antigens simultaneously (EC50 = 11.48 nM; EC50 = 0.02462 μg/mL for dual cell binding)[1].
Amulirafusp alfa has higher binding affinity for purified CD20 (2.45 nM) than for purified CD47 (4.91 nM)[1].
Amulirafusp alfa binds to multiple B-cell lymphoma cell lines, human PBMC, and cynomolgus monkey PBMC, shows minimal binding to human RBC (no hemagglutination), and cross-reacts with human and cynomolgus CD47 but not mouse or rat CD47[1].
Amulirafusp alfa significantly inhibits apoptosis of Jurkat-CSR cells via SIRPα/CD47 pathway blockade, with an IC50 of 4.046 nM[1].
Amulirafusp alfa induces potent ADCC, ADCP, and CDC against Raji, Daudi, Jeko-1, Ramos, SU-DHL-4, and SU-DHL-10 B-cell lymphoma cells, with stronger ADCC than rituximab, greater phagocytic activity against lymphoma cells than rituximab, and reduced activity against normal cells[1].
Amulirafusp alfa (10 μg/mL; 30 min) potently induces antibody-dependent cellular phagocytosis of TMD-8 and U-2932 ABC-DLBCL cells in vitro, with efficacy increasing as the effector-to-tumor cell ratio rises[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Amulirafusp alfa (IMM-0306) (5 mg/kg; i.v.; weekly; 4 weeks) achieves 89.98-92.7% tumor growth inhibition in CB17-SCID mice bearing orthotopic Raji xenografts[1].
Amulirafusp alfa (IMM-0306) (1 mg/kg; i.v.; weekly; 4 weeks) reduces tumor bioluminescence intensity in CB17-SCID mice bearing orthotopic Raji-luc xenografts[1].
Amulirafusp alfa (IMM-0306) (2.5 mg/kg; i.v.; Days 2, 4, 6, 9, 11, and 13) exerts dose-dependent antitumor efficacy in ABC-DLBCL xenograft models, with significantly enhanced activity in tumors with high IL-16 expression, reducing mean tumor volume to ~350 mm3 in pre-IL-16-overexpressing U-2932 xenografts by Day 14[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CB17-SCID mice (subcutaneous xenograft via 2×106 Daudi cells inoculation)[1]
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Dosage:1.5 mg/kg
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Administration:i.v.; weekly; 3 weeks
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Result:Achieved 100% complete tumor remission.
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Animal Model:CB17-SCID mice (orthotopic xenograft via 5×106 Raji cells tail vein inoculation)[1]
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Dosage:5 mg/kg
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Administration:i.v.; weekly; 4 weeks
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Result:Achieved 89.98% tumor growth inhibition.
Achieved 92.7% tumor growth inhibition.
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Animal Model:CB17-SCID mice (orthotopic xenograft via Raji-luc cells tail vein inoculation)[1]
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Dosage:1 mg/kg; 3 mg/kg (lenalidomide combination)
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Administration:i.v.; weekly; 4 weeks; p.o. (lenalidomide on day 0 and days 5-27)
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Result:Significantly reduced tumor bioluminescence intensity compared to vehicle control.
Reduced tumor bioluminescence intensity to a lower level than amulirafusp alfa monotherapy, lenalidomide monotherapy, and rituximab plus lenalidomide when combined with lenalidomide.
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Animal Model:NOD SCID (T- and B-lymphocyte dysfunction, low natural killer cell and complement binding capacity)[4]
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Dosage:2.5 mg/kg
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Administration:i.v.; Days 2, 4, 6, 9, 11, and 13
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Result:Reduced mean tumor volume to ~700 mm3 by Day 14 in mice inoculated with empty vector control U-2932 cells, compared to ~1000 mm3 in the control group.
Reduced mean tumor volume to ~350 mm3 by Day 14 in mice inoculated with pre-IL-16-overexpressing U-2932 cells, compared to ~1600 mm3 in the control group.
Exerted a significantly stronger therapeutic effect in pre-IL-16-overexpressing U-2932 cell-inoculated mice than in empty vector group mice.
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Q61735-1 & P11836
Unconjugated
The product can be reconstituted/diluted with sterile PBS or saline.
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IgG1-kappa-[PROTEIN]2-in-VH
ELISA, FACS, Functional assay
Chemical Information
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CAS No. 2850355-94-9
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SMILES
[Amulirafusp alfa]
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Synonyms
IMM-0306
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Shipping
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
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Data Sheet (267 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
References
[1]. Yu J, et al. IMM0306, a fusion protein of CD20 mAb with the CD47 binding domain of SIRPα, exerts excellent cancer killing efficacy by activating both macrophages and NK cells via blockade of CD47-SIRPα interaction and FcɣR engagement by simultaneously binding to CD47 and CD20 of B cells. Leukemia. 2023 Mar;37(3):695-698. [Content Brief]
[3]. Yang J, et al. Safety and efficacy of amulirafusp alfa (IMM0306), a fusion protein of CD20 monoclonal antibody with the CD47 binding domain of SIRPα, in patients with relapsed or refractory B-cell non-Hodgkin lymphoma: a phase 1/2 study. Journal of hematology & oncology. 2024 Dec 18;17(1):123. [Content Brief]
[4]. Guan X, et al. Lymphoma cell-driven IL-16 is expressed in activated B-cell-like diffuse large B-cell lymphomas and regulates the pro-tumor microenvironment. Haematologica. 2025 Feb 1;110(2):425-438. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)