Atrosimab (Synonyms: ATM-001)

Cat. No.: HY-P991049 Purity: 99%: Data Sheet
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Atrosimab is an Fv-Fc1K fusion protein with an EC₅₀ value of 0.37 nM against humans. Atrosimab inhibits TNF-induced TNFR1 activation, release of IL-6 and IL-8, and cell death, and alleviates neuroinflammation. Atrosimab is applicable to research related to inflammatory diseases, neurodegenerative diseases, acute and chronic inflammation, experimental arthritis, non-alcoholic steatohepatitis, and experimental autoimmune encephalomyelitis.

For research use only. We do not sell to patients.

Size	Stock	Quantity
1 mg	In-stock	Estimated Time of Arrival: December 31
5 mg	In-stock	Estimated Time of Arrival: December 31
10 mg	In-stock	Estimated Time of Arrival: December 31
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TNFRSF1A/CD120a TNFRSF3/CD18 TNFRSF4 TNFRSF5/CD40 TNFRSF6/Fas/CD95 TNFRSF7/CD27 TNFRSF8/CD30 TNFRSF9/4-1BB/CD137 TNFRSF10B/DR5/CD262 TNFRSF12A/TWEAK TNFRSF16/NGF Receptor/CD271 TNFRSF18/GITR/CD357

Biological Activity
Purity & Documentation
References
Customer Review

Description

Isotype

Fv-Fc

Species Reactivity

Human

In Vitro

Atrosimab (serial dilutions; 4-128 nM) binds purified human TNFR1-Fc with high affinity, and lacks binding to human complement protein C1q and human Fcγ receptors Ia, IIb, IIIa^[1].
Atrosimab (100 nM; 1, 3, 7 days) exhibits good stability in human plasma for at least 7 days and has an aggregation temperature of 64°C^[1].
Atrosimab (serial dilutions; 16-20 h, 24 h) potently inhibits TNF-mediated TNFR1 activation in HeLa, HT1080, and Kym-1 cells, with IC₅₀ values of 54.5 nM, 24.2 nM, and 16.2 nM, respectively^[1].
Atrosimab (serial dilutions; 16-20 h) does not exhibit TNFR1 agonistic activity in HT1080 cells even when cross-linked by three different goat anti-human IgG sera^[1].
Atrosimab (24 h) does not affect spontaneous or glutamate-induced altered firing rates of huTNFR1-k/i mouse embryonic day 14 primary cortical neurons after 24 h incubation^[2].
Atrosimab (100 μg; heated from 35°C to 80°C with 2 min equilibration per 1°C interval; 2-500 nM; up to 9 months) is highly thermally and long-term stable, binds selectively and with high affinity to human, rhesus, and cynomolgus TNFR1 (but not mouse/rat TNFR1 or any TNFR2), and recognizes an epitope on human TNFR1 that includes residues P23, L67, R68, H69, and Q24^[3].
Atrosimab (up to 1000 nM; 16-20 h at 37°C, 5% CO₂; 1-7 days at 37°C in 50% human serum) potently and dose-dependently inhibits TNF-induced IL-8 release in HT1080 cells with IC₅₀ values of 21.9-34.9 nM, does not exhibit agonistic activity in these cells, and maintains functional stability after incubation in human serum at 37°C for up to 7 days^[3].
Atrosimab (100 μg/mL; 24 h) inhibits TNF-induced VCAM-1 and ICAM-1 expression in hCMEC/D3 human brain microvascular endothelial cells^[3].

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

ELISA Assay^[1]

Cell Line:	HT1080 cells
Concentration:	serial dilutions of Atrosimab; ~15.8 nM (constant anti-human IgG serum)
Incubation Time:	16-20 h
Result:	Showed no induction of IL-8 release across all tested concentrations, indicating no cross-linking-mediated TNFR1 agonistic activity.

Parmacokinetics

Species	Dose	Route	T_1/2 (Distribution)	T_1/2β	AUC_0-t	C₀	V_ss	CL
Mice^[1]	400 μg	i.v.	2.2 h	41.7 h	5856.0 μg·h/mL	324.7 μg/mL	3.4 μg/mL	0.29 μg/mL
Mice^[3]	30.0 mg/kg	i.v.	2.26 h	32.77 h	6989.7 μg·h/mL	/	/	/
Mice^[3]	1.0 mg/kg	i.v.	1.05 h	31.37 h	365.78 μg·h/mL	/	/	/
Mice^[3]	30.0 mg/kg	s.c.	/	33.7 h	6190.7 μg·h/mL	/	/	/
Mice^[3]	1.0 mg/kg	s.c.	/	54.56 h	321.83 μg·h/mL	/	/	/
Mice^[3]	30.0 mg/kg	i.v.	0.66 h	31.52 h	7983.8 μg·h/mL	/	/	/
Mice^[3]	1.0 mg/kg	i.v.	5.41 h	9.52 h	177.8 μg·h/mL	/	/	/
Mice^[3]	30.0 mg/kg	s.c.	/	41 h	6816.7 μg·h/mL	/	/	/
Mice^[3]	1.0 mg/kg	s.c.	/	16.75 h	214.07 μg·h/mL	/	/	/

In Vivo

Atrosimab (3 μg; stereotactic co-injection into NBM) improves long-term associative memory, reduces neuronal and cholinergic loss, and decreases glial activation and lesion size in an NMDA-induced acute neurodegeneration mouse model^[2].
Atrosimab (30 mg/kg; i.v.; single dose) potently blocks acute TNF-induced inflammatory responses in huTNFR1-k/i mice^[3].
Atrosimab (20-80 mg/kg; s.c.; twice weekly; 11 weeks) prevents arthritis development in a prophylactic setting and Atrosimab (5-45 mg/kg; s.c.; twice weekly; 6 weeks) alleviates established arthritis with dose-dependent efficacy in Tg197hTNFR1KI mice^[3].
Atrosimab (45 mg/kg; i.p.; twice weekly; 8 weeks) alleviates liver fibrosis, steatosis, and apoptotic injury in a huTNFR1-k/i mouse model of NASH^[3].
Atrosimab (30-60 mg/kg; i.p.; single doses on days 1, 4, 8, 12 of manifest disease) ameliorates motor symptoms, demyelination, and axonal injury in a huTNFR1-k/i mouse model of EAE, with 30 mg/kg being sufficient for maximal therapeutic activity^[3].

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

Animal Model:	huTNFR1-k/i (7-month-old male; C57Bl/6J background; NMDA-induced acute cholinergic neurodegeneration via stereotactic injection into NBM)^[2]
Dosage:	3 μg
Administration:	stereotactic co-injection into NBM; infused at 0.1 μl/min at two dorsoventral depths: 0.3 μl at -0.44 mm and 0.3 μl at -0.46 mm relative to Bregma; total volume 0.6 μl
Result:	Increased post-shock latency to 274.8 s in passive avoidance paradigm, indicating improved long-term associative memory.\nPrevented significant body weight loss, with mean body weight change of -2.43 g from surgery to perfusion.\nIncreased surface area of ChAT-positive cholinergic fibers in layer V of somatosensory cortex to 11.04%.\nIncreased ratio of cholinergic neurons in lesioned vs. non-lesioned NBM hemisphere to 0.14.\nIncreased ratio of NeuN-positive neuronal surface area in lesioned vs. non-lesioned somatosensory cortex layer V to 0.48.\nReduced volume of IBA-1-positive activated microglia/lesion size to 0.373 mm³.\nReduced ratio of CD68 mean intensity (lesioned vs. non-lesioned NBM hemisphere) to 1.22.\nReduced ratio of GFAP mean intensity (lesioned vs. non-lesioned NBM hemisphere) to 2.51. Showed no significant effect on short-term spatial memory, anxiety-like behavior, locomotor activity, or hippocampal synapsin-1 levels.

Animal Model:	huTNFR1-k/i (C57BL/6 background)^[3]
Dosage:	30 mg/kg
Administration:	i.v.; single dose
Result:	Completely blocked TNF-induced body weight loss.\nSignificantly reduced serum IL-6 levels at 1 hour and 6 hours post-TNF injection to almost baseline levels.\nSignificantly reduced TNF-induced systemic CRP levels at 6 hours post-TNF injection compared to control-treated mice.

Animal Model:	Tg197hTNFR1KI^[3]
Dosage:	20-80 mg/kg (prophylactic setting); 5-45 mg/kg (therapeutic setting)
Administration:	s.c.; twice weekly; 11 weeks (prophylactic setting); 6 weeks (therapeutic setting)
Result:	Prevented development of arthritic disease, prevented disease-associated inhibition of body weight gain, and resulted in no histopathological changes beyond the level of 4-week-old control mice (all doses, prophylactic setting).\nHalted disease progression (5 mg/kg, therapeutic setting).\nShowed improved therapeutic activity comparable to approved anti-TNF therapeutics (15 mg/kg, 45 mg/kg, therapeutic setting).\nImproved joint histopathology, with histopathological scores below the level of 9-week-old control mice (all doses, therapeutic setting).

Animal Model:	huTNFR1-k/i (male)^[3]
Dosage:	45 mg/kg
Administration:	i.p.; twice weekly; 8 weeks
Result:	Significantly reduced liver fibrosis (assessed by Sirius Red staining).\nReduced liver steatosis (assessed by Oil Red O staining).\nDecreased activated caspase-3-positive cells (a marker of apoptotic liver injury) compared to saline-treated mice.

Animal Model:	huTNFR1-k/i (female, 6-8 weeks old)^[3]
Dosage:	30-60 mg/kg
Administration:	i.p.; single doses on days 1, 4, 8, 12 of manifest disease
Result:	Ameliorated EAE motor symptoms.\nReduced cumulative EAE score.\nPrevented disease-associated weight loss.\nReduced cumulative weight loss.\nSignificantly reduced spinal cord demyelination (assessed by Luxol fast blue staining).\nSignificantly reduced axonal injury (assessed by amyloid precursor protein accumulation) compared to control-treated mice.\nShowed no efficacy difference between the 30 mg/kg and 60 mg/kg doses.

Clinical Trial

Gene ID

7132 [NCBI]

Accession

P19438

Application

ELISA, FACS, Functional assay

Conjugated

Unconjugated

Reconsititution

The product can be reconstituted/diluted with sterile PBS or saline.

Molecular Weight

72.338 kDa

Appearance

Liquid

Color

Colorless to light yellow

SMILES

[Atrosimab]

Shipping

Shipping with dry ice.

Formulation

Please refer to the lot-specific COA for specific buffer information.

Storage

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

Format

Fv-Fc1κ

Biological Activity

Loaded Atrosimab on ProA biosensor, can bind TNFR-1/CD120a Protein, Human (HEK293, His, HY-P700263) with an affinity constant of 2.076E-09 M as determined in BLI assay.

Purity & Documentation

Purity: 99%

Select Batch:

Data Sheet (268 KB) SDS (251 KB)

COA (232 KB) SDS-PAGE (91 KB) SEC-HPLC (170 KB)

Inhibitory Antibodies User Guide (603 KB)

References

[1]. Richter F, et al. Improved monovalent TNF receptor 1-selective inhibitor with novel heterodimerizing Fc. MAbs. 2019;11(4):653-665. [Content Brief]

[2]. Ortí-Casañ N, et al. The TNFR1 antagonist Atrosimab reduces neuronal loss, glial activation and memory deficits in an acute mouse model of neurodegeneration. Sci Rep. 2023;13(1):10622. Published 2023 Jun 30. [Content Brief]

[3]. Richter F, et al. The TNFR1 Antagonist Atrosimab Is Therapeutic in Mouse Models of Acute and Chronic Inflammation. Front Immunol. 2021;12:705485. Published 2021 Jul 7. [Content Brief]

Atrosimab Related Classifications

Metabolic Disease Inflammation/Immunology

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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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