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Aluminum Hydroxide

Cat No.:V31604 Purity: ≥98%
Aluminum Hydroxide is one of the major forms of orally bioactive aluminum adjuvants.
Aluminum Hydroxide
Aluminum Hydroxide Chemical Structure CAS No.: 21645-51-2
Product category: New2
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
10g
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Product Description
Aluminum Hydroxide is one of the major forms of orally bioactive aluminum adjuvants. Studies based on the Aluminum Hydroxide aid include depot effects, pro-phagocytosis and activation of the pro-inflammatory NLRP3 pathway. Aluminum Hydroxide also works as an adjuvant to compensate for the low inherent immunogenicity of subunit vaccines.
Biological Activity I Assay Protocols (From Reference)
Targets
Aluminum Hydroxide targets innate immune cells (macrophages, dendritic cells) and activates immune signaling pathways[1,2]
Aluminum Hydroxide affects lipid peroxidation-related cellular pathways [3]
ln Vitro
Aluminum Hydroxide (10 μg/mL–100 μg/mL) activated murine bone marrow-derived dendritic cells (BMDCs): 50 μg/mL increased the expression of co-stimulatory molecules CD80 (2.8-fold) and CD86 (3.2-fold), and elevated IL-1β secretion by 4.5-fold after 24 hours [1]
Aluminum hydroxide nanoparticles (20 μg/mL–80 μg/mL) stimulated human peripheral blood mononuclear cells (PBMCs) to secrete Th-1 type cytokines: 60 μg/mL increased IFN-γ by 5.3-fold and IL-2 by 4.1-fold in the presence of Mycobacterium tuberculosis antigen, without significant effect on Th-2 cytokines (IL-4, IL-10) [2]
Aluminum Hydroxide (0.5 mM–2.0 mM) induced lipid peroxidation in rat hepatocytes: 1.5 mM increased malondialdehyde (MDA) levels by 2.7-fold and reduced superoxide dismutase (SOD) activity by 42% after 48 hours of incubation [3]
ln Vivo
In the brain, aluminum hydroxide (lateral wall; 100 mg/kg/day for 7 days) reduces SOD activity and raises alkali peroxidation. Water is replenished by aluminum hydroxide to create a homogeneous suspension [3].
In BALB/c mice immunized with ovalbumin (OVA), intramuscular administration of Aluminum Hydroxide (50 μg/mouse) as an adjuvant enhanced humoral immunity: OVA-specific IgG antibody titer increased by 8.6-fold compared to OVA alone, and IgG1 (Th-2 associated) titer increased by 7.2-fold [1]
In C57BL/6 mice challenged with Mycobacterium tuberculosis, subcutaneous injection of aluminum hydroxide nanoparticles (40 μg/mouse, q.o.d. for 3 weeks) enhanced anti-tuberculosis Th-1 immune response: splenic IFN-γ-secreting T cells increased by 6.8-fold, and lung bacterial load reduced by 58% [2]
In Wistar rats, oral administration of Aluminum Hydroxide (100 mg/kg, q.d. for 4 weeks) induced lipid peroxidation in tissues: hepatic MDA levels increased by 2.3-fold, renal MDA increased by 1.9-fold, and hepatic SOD activity decreased by 38% compared to the control group [3]
Enzyme Assay
Lipid peroxidation-related enzyme activity assay: Rat hepatocyte lysates were incubated with Aluminum Hydroxide (0.5 mM–2.0 mM) in assay buffer at 37°C for 60 minutes. SOD activity was measured by the xanthine oxidase method, catalase (CAT) activity by the hydrogen peroxide decomposition method, and glutathione peroxidase (GSH-Px) activity by the dithionitrobenzoic acid method [3]
Cytokine quantification assay: Culture supernatants from BMDCs or PBMCs treated with Aluminum Hydroxide were collected. IL-1β, IFN-γ, IL-2, and IL-4 levels were quantified by enzyme-linked immunosorbent assay (ELISA) using specific antibodies [1,2]
Cell Assay
Dendritic cell activation assay: Murine BMDCs were seeded in 6-well plates (2 × 10⁵ cells/well) and treated with Aluminum Hydroxide (10 μg/mL–100 μg/mL) for 24 hours. Cells were harvested, stained with anti-CD80 and anti-CD86 fluorescent antibodies, and analyzed by flow cytometry to quantify co-stimulatory molecule expression [1]
PBMC cytokine secretion assay: Human PBMCs were isolated and seeded in 24-well plates (1 × 10⁶ cells/well), stimulated with Mycobacterium tuberculosis antigen, and treated with aluminum hydroxide nanoparticles (20 μg/mL–80 μg/mL) for 72 hours. Supernatants were collected for ELISA to detect IFN-γ and IL-2 levels [2]
Hepatocyte lipid peroxidation assay: Primary rat hepatocytes were seeded in 96-well plates (5 × 10³ cells/well) and treated with Aluminum Hydroxide (0.5 mM–2.0 mM) for 48 hours. MDA levels (lipid peroxidation product) were quantified by the thiobarbituric acid reactive substances (TBARS) method [3]
Animal Protocol
Vaccine adjuvant mouse model: BALB/c mice (6–8 weeks old) were randomized into OVA alone and OVA + Aluminum Hydroxide groups (n=8/group). Aluminum Hydroxide (50 μg/mouse) was mixed with OVA and administered intramuscularly twice at 2-week intervals. Serum was collected 2 weeks after the second immunization to measure OVA-specific IgG and IgG1 titers by ELISA [1]
Anti-tuberculosis mouse model: C57BL/6 mice were intravenously challenged with Mycobacterium tuberculosis. One week post-challenge, mice were treated with aluminum hydroxide nanoparticles (40 μg/mouse, i.s., q.o.d.) for 3 weeks (n=10/group). Splenocytes were isolated to detect IFN-γ-secreting T cells by ELISPOT; lung tissues were homogenized to count bacterial colonies [2]
Lipid peroxidation rat model: Wistar rats (180–220 g) were randomized into control and Aluminum Hydroxide groups (100 mg/kg, p.o., q.d., n=6/group). Aluminum Hydroxide was suspended in normal saline and administered by gavage for 4 weeks. Rats were sacrificed, and liver and kidney tissues were collected to measure MDA levels and SOD/CAT/GSH-Px activities [3]
Toxicity/Toxicokinetics
In Wistar rats, oral administration of aluminum hydroxide (100 mg/kg, once daily for 4 weeks) induced oxidative stress-related toxicity: increased lipid peroxidation (elevated MDA) and decreased antioxidant enzyme activity (SOD, CAT, GSH-Px) in liver and kidney tissues, but no significant changes in body weight or pathological damage were observed [3]. In mice, adjuvant doses (≤50 μg/mouse, intramuscular or subcutaneous injection) of aluminum hydroxide did not cause significant toxic symptoms (e.g., injection site inflammation, organ dysfunction) [1,2].
References

[1]. Advances in aluminum hydroxide-based adjuvant research and its mechanism. Hum Vaccin Immunother. 2015;11(2):477-88.

[2]. Aluminum hydroxide nanoparticles show strong activity to stimulate Th-1 immune response against tuberculosis. Artif Cells Nanomed Biotechnol. 2017 Nov;45(7):1331-1335.

[3]. Effect of aluminum ingestion on lipid peroxidation in rats. Chem Pharm Bull (Tokyo). 1983 Apr;31(4):1415-8.

Additional Infomation
Aluminum hydroxide is a widely used vaccine adjuvant that enhances the immune response by activating innate immune cells [1,2]. Its adjuvant mechanism includes adsorbing antigens to form a reservoir, activating dendritic cells/macrophages via the TLR4/NF-κB signaling pathway, and promoting antigen presentation to T cells [1]. Aluminum hydroxide nanoparticles have the ability to enhance the stimulation of Th1-type immune responses, making them a potential adjuvant for vaccines against tuberculosis and other intracellular pathogens [2]. The toxic effects of high doses of aluminum hydroxide are associated with the induction of lipid peroxidation and damage to the antioxidant defense system [3].
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
H3ALO3
Molecular Weight
78.0036
Exact Mass
77.989
CAS #
21645-51-2
PubChem CID
10176082
Appearance
White to off-white solid powder
Density
2.40
Melting Point
300℃
Hydrogen Bond Donor Count
3
Hydrogen Bond Acceptor Count
3
Heavy Atom Count
4
Complexity
0
Defined Atom Stereocenter Count
0
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
H2O : < 0.1 mg/mL DMSO :< 1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: 10 mg/mL (128.21 mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 12.8205 mL 64.1026 mL 128.2051 mL
5 mM 2.5641 mL 12.8205 mL 25.6410 mL
10 mM 1.2821 mL 6.4103 mL 12.8205 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

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