Aducanumab manufacturers
- Aducanumab
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- $189.00
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2026-07-13
- CAS:1384260-65-4
- Purity: 95.00%
- Supply Ability: 10g
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| | Aducanumab Basic information |
| Product Name: | Aducanumab | | Synonyms: | Aducanumab;AducanumabQ: What is
Aducanumab Q: What is the CAS Number of
Aducanumab;Research Grade Aducanumab(DHC12504);Aducanumab (anti-APP);BIIB037;Research Grade Aducanumab | | CAS: | 1384260-65-4 | | MF: | | | MW: | 0 | | EINECS: | | | Product Categories: | | | Mol File: | Mol File | ![Aducanumab Structure]() |
| | Aducanumab Chemical Properties |
| storage temp. | Store at -80°C, Aliquots should be stored at the same temperature after first use to avoid multiple freeze-thaws | | form | Liquid | | color | Colorless to light yellow |
| | Aducanumab Usage And Synthesis |
| History | Aducanumab(brand name Aduhelm) was discovered by Biogen and Eisai, is an anti-amyloid drug designed to treat Alzheimer's disease. It is a monoclonal antibody that targets aggregated forms (plaque)[3][4] of amyloid beta (Aβ) found in the brains of people with Alzheimer's disease to reduce its buildup. Granted accelerated approval by the United States Food and Drug Administration (FDA) in June 2021, aducanumab is the first AD treatment to receive formal regulatory clearance since 2003. | | Uses | Aducanumab (BIIB037) is a human monoclonal antibody that selectively targets aggregated amyloid-beta (Aβ). Aducanumab shows brain penetration, and can be used for Alzheimer's disease (AD) research[1]. | | Enzyme inhibitor | This high-affinity, fully human IgG1 monoclonal antibody (MW = 149.5 kDa; CAS 1384260-65-4), also known by the developmental code name BIIB037, selectively targets aggregated forms of b-amyloid protein (EC50 = 0.1 nM), while showing weak binding to Ab monomer. In the brains of transgenic mice, aducanumab preferentially binds to parenchymal Aβ over vascular Aβ deposits, consistent with the lack of effect on vascular Aβ following chronic dosing. Aducanumab dose-dependently reduces amyloid deposition in six cortical regions of the brain. chAducanumab, a murine IgG2a/κ chimeric analogue, dose-dependently reduces Aβ measured in brain homogenates by up to 50% relative to the vehicle control in the diethylamine fraction that extracted soluble monomeric and oligomeric forms of Aβ40 and Aβ42, and in the guanidine hydrochloride fraction that extracted insoluble Aβ fibrils. The clearance of Aβ deposits was accompanied by enhanced recruitment of microglia. Together with the reduced potency of the aglycosylated form of chaducanumab and the ex vivo phagocytosis data, such findings suggest that FcγR-mediated microglial recruitment and phagocytosis played an important role in Aβ clearance in these models. Activated microglia appeared to encapsulate the remaining central dense core of plaques in treated animals, possibly isolating them from the surrounding neurophil. | | in vivo | Aducanumab (30 mg/kg, i.p., single dose) binds all morphological types of brain Aβ plaques in 22-month-old Tg2576 transgenic mice, including diffuse Aβ deposits and compact Aβ plaques[1].
Aducanumab (0.3-30 mg/kg, i.p., weekly, 6 months) reduces soluble and insoluble Aβ in a dose-dependent manner in 9.5- to 15.5-month-old Tg2576 transgenic mice[1].
Aducanumab (10 mg/kg, i.p., weekly, 6 months) restores intracellular calcium to control levels in 18-month-old Tg2576 mice[2].
Aducanumab (0.4-1 mg/mL, ICV, 20 min) leads to rapid decrease in amyloid burden, plaque clearance in Tg2576 mice[2].
| Animal Model: | 9.5- to 15.5-month-old Tg2576 transgenic mice [1] | | Dosage: | 0.3-30 mg/kg | | Administration: | Intraperitoneal injection (i.p.), weekly, 6 months | | Result: | Increased recruitment of Iba-1-positive microglia to Aβ plaques.
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| Animal Model: | 18-month-old Tg2576 mice[2] | | Dosage: | 10 mg/kg | | Administration: | Intraperitoneal injection (i.p.), weekly, 6 months | | Result: | Restored neurite baseline calcium to control levels.
Decreased the number of neurites with elevated levels of calcium after 2 weeks.
Decreased the percentage of cell bodies with calcium overload.
Restored the levels of VILIP and SERCA to control levels.
Increased the cell numbers of NR1 and NR2A.
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| Animal Model: | 22-month-old transgenic Tg2576 mice[2] | | Dosage: | 0.4-1 mg/mL | | Administration: | Intracerebroventricular injection (ICV), 20 min | | Result: | Decreased the number of amyloid plaque.
Decreased the size of the remaining individual plaques.
Reduced amyloid plaque burden.
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| | References | [1] Sevigny J, et al. The antibody aducanumab reduces Aβ plaques in Alzheimer's disease. Nature. 2016 Sep 1;537(7618):50-6. DOI:10.1038/nature19323
[2] Kastanenka KV, et al. Immunotherapy with Aducanumab Restores Calcium Homeostasis in Tg2576 Mice. J Neurosci. 2016 Dec 14;36(50):12549-12558. DOI:10.1523/JNEUROSCI.2080-16.2016 |
| | Aducanumab Preparation Products And Raw materials |
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