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D-Galactosamine HCl

Cat No.:V19714 Purity: ≥98%
D(+)-Galactosamine (D-Galactosamine) HCl is an established experimental toxin that causes liver damage primarily through the production of free radicals and depletion of UTP nucleotides.
D-Galactosamine HCl
D-Galactosamine HCl Chemical Structure CAS No.: 1772-03-8
Product category: New1
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
250mg
500mg
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Other Forms of D-Galactosamine HCl:

  • D(+)-Galactosamine-13C HCl
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Product Description
D(+)-Galactosamine (D-Galactosamine) HCl is an established experimental toxin that causes liver damage primarily through the production of free radicals and depletion of UTP nucleotides. D(+)-Galactosamine HCl intoxication can also lead to renal insufficiency, so renal failure is often associated with end-stage liver damage. Lipopolysaccharide/D(+)-Galactosamine-induced acute liver injury is a known animal model of fulminant liver failure.
D-Galactosamine HCl (CAS 1772-03-8) is an amino sugar derivative of D-galactose that serves as an established experimental hepatotoxin. It is widely used in preclinical research to induce liver injury, primarily through the generation of free radicals and the depletion of uridine triphosphate (UTP) nucleotides in hepatocytes. This compound is commonly utilized alone or in combination with lipopolysaccharide (LPS) to create a well-characterized animal model of fulminant hepatic failure. With the molecular formula C6H14ClNO5 and a molecular weight of 215.63 g/mol, D-Galactosamine HCl is a white to off-white solid powder that is soluble in water. Its mechanism of toxicity involves the depletion of UTP, which disrupts RNA synthesis and leads to hepatocellular damage. The compound is strictly intended for research purposes and is not for human use.
Biological Activity I Assay Protocols (From Reference)
Targets
D-Galactosamine HCl does not have a single defined molecular target but exerts its effects through metabolic disruption. Its primary mechanism involves the depletion of uridine triphosphate (UTP) nucleotides in hepatocytes, which is caused by the formation of galactosamine-1-phosphate and the subsequent trapping of uridine nucleotides. This depletion leads to an inhibition of RNA and protein synthesis, ultimately resulting in cell death. The compound also induces the generation of free radicals, contributing to oxidative stress and mitochondrial dysfunction. Additionally, D-Galactosamine HCl intoxication can lead to renal dysfunction, which is often associated with end-stage liver damage.
ln Vitro
In primary cultured hepatocytes, D(+)-galactosamine (5 mM, 0-24 h) hydrochloride causes DNA fragmentation, caspase-3 activation, and engraftment and bridging [3].
In vitro, D-Galactosamine HCl causes significant hepatocyte damage in primary cultured hepatocytes. Treatment with 5 mM of the compound for 0-24 hours results in DNA fragmentation, caspase-3 activation, and cellular engraftment and bridging. These effects are indicative of apoptosis and necrosis, confirming the compound's direct cytotoxic action on liver cells. The mechanism involves the depletion of UTP nucleotides and the generation of free radicals, which disrupt cellular metabolism and lead to cell death. D-Galactosamine HCl is also used in vitro to study the protective effects of various compounds against hepatotoxicity.
ln Vivo
When lipopolysaccharide (LPS, 10 μg/kg) and D(+)-galactosamine (700 mg/kg, ip) hydrochloride are coupled, an acute liver injury model can be induced, exhibiting symptoms like anorexia, convulsions, syncope, and depression. Inducing C57BL/6J indirectly, kit 40.0% (36/90) requires D(+)-galactosamine (400 mg/kg, ip) hydrochloride in combination with lipopolysaccharide (LPS, 10 μg/kg) [1].
In vivo, D-Galactosamine HCl is a potent hepatotoxin that induces acute liver injury. When administered intraperitoneally (i.p.) at a dose of 700 mg/kg in combination with lipopolysaccharide (LPS, 10 μg/kg), it produces a model of acute liver failure characterized by symptoms such as anorexia, convulsions, syncope, and depression. In C57BL/6J mice, a dose of 400 mg/kg D-Galactosamine HCl together with LPS (10 μg/kg) induces acute liver failure accompanied by hepatic necrosis. This treatment leads to significant increases in serum ALT and AST levels, as well as elevated concentrations of inflammatory cytokines including TNF-α, IFN-γ, IL-1β, IL-6, and IL-18. The LPS/D-Galactosamine model is a widely accepted and reproducible system for studying fulminant hepatic failure and evaluating hepatoprotective agents.
Enzyme Assay
In vitro enzyme/receptor binding assays for D-Galactosamine HCl are not typical, as the compound is not a direct enzyme inhibitor. However, its effects are studied through metabolic and cytotoxicity assays. Researchers often measure cellular UTP levels, ATP levels, and markers of oxidative stress such as reactive oxygen species (ROS) and lipid peroxidation. The compound's ability to induce DNA fragmentation and caspase-3 activation is also assessed as markers of apoptosis. These assays help elucidate the compound's mechanism of hepatotoxicity.
Cell Assay
D-Galactosamine HCl is extensively used in cell-based assays to study hepatotoxicity and the effects of potential hepatoprotective agents. Primary hepatocyte cultures are the most common model, where cells are treated with the compound (typically 5 mM) for varying durations (0-24 hours). Endpoints include cell viability, DNA fragmentation, caspase-3 activation, and the measurement of inflammatory cytokine production. These studies are crucial for understanding the mechanisms of liver damage and for screening compounds with potential therapeutic benefits against liver injury.
Animal Protocol
Animal/Disease Models: C57BL/6J mice [2]
Doses: 400 mg/kg, administered together with lipopolysaccharide (LPS, 10 μg/kg): ip
Experimental Results: Induced acute liver failure model, accompanied by necrosis. in the liver. Serum ALT and AST levels and serum concentrations of inflammatory cytokines, such as TNF-α, IFN-γ, IL-1β, IL-6, and IL-18, were increased.
In vivo animal studies using D-Galactosamine HCl are well-established, particularly the LPS/D-Galactosamine model of acute liver failure. In this model, mice (typically C57BL/6J) are given an intraperitoneal injection of D-Galactosamine HCl (400-700 mg/kg) along with LPS (10 μg/kg). The animals are then monitored for signs of liver failure, and serum and tissue samples are collected for analysis. Key endpoints include serum ALT and AST levels, hepatic necrosis, and the production of inflammatory cytokines. This model is extensively used to evaluate the efficacy of hepatoprotective drugs and to study the pathophysiology of fulminant hepatic failure.
ADME/Pharmacokinetics
Pharmacokinetic properties of D-Galactosamine HCl are primarily studied in the context of its toxicological effects. Following intraperitoneal administration, the compound is rapidly taken up by the liver, where it exerts its hepatotoxic effects. The pharmacokinetic profile is characterized by the rapid depletion of UTP nucleotides and the subsequent disruption of RNA synthesis. For storage, the powder should be kept at -20°C for up to 3 years or at 4°C for up to 2 years; in solution, it can be stored at -80°C for 6 months or at -20°C for 1 month.
Toxicity/Toxicokinetics
D-Galactosamine HCl is a toxic compound with a well-characterized toxicological profile. It is a potent hepatotoxin that causes liver damage through free radical generation and UTP depletion. The compound also induces renal dysfunction, and renal failure is often associated with end-stage liver damage. Its toxicity is dose-dependent, and it is primarily used as a research tool to induce liver injury. The compound should be handled with appropriate safety precautions in laboratory settings, as it is not intended for human or veterinary use.
References

[1]. Inhibition of PI3K/AKt/mTOR signaling pathway protects against d-galactosamine/lipopolysaccharide-induced acute liver failure by chaperone-mediated autophagy in rats. Biomed Pharmacother. 2017 Aug;92:544-553.

[2]. AMSC-derived exosomes alleviate lipopolysaccharide/d-galactosamine-induced acute liver failure by miR-17-mediated reduction of TXNIP/NLRP3 inflammasome activation in macrophages. EBioMedicine. 2018 Oct;36:140-150.

[3]. PGE1 abolishes the mitochondrial-independent cell death pathway induced by D-galactosamine in primary culture of rat hepatocytes. J Gastroenterol Hepatol. 2005 Jan;20(1):108-16.

Additional Infomation
D-(+)-galactosamine hydrochloride is a hexose.
See also: Galactosamine hydrochloride (note moved to).
D-Galactosamine HCl is a research compound with no approved human therapeutic use. Its primary value lies in its role as an experimental hepatotoxin for inducing acute liver injury in animal models, particularly the LPS/D-Galactosamine model of fulminant hepatic failure. This model is essential for studying the pathophysiology of liver disease and for evaluating the efficacy of potential hepatoprotective agents. The compound is also used in vitro to study the mechanisms of hepatocyte injury and to screen for compounds that can protect against liver damage.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C6H14CLNO5
Molecular Weight
215.6321
Exact Mass
215.056
CAS #
1772-03-8
Related CAS #
D(+)-Galactosamine-13C hydrochloride;478518-54-6
PubChem CID
2723866
Appearance
White to off-white solid powder
Boiling Point
532.5ºC at 760 mmHg
Melting Point
182-185 °C (dec.)(lit.)
Flash Point
275.8ºC
Vapour Pressure
5.53E-10mmHg at 25°C
Index of Refraction
96 ° (C=1, H2O)
Hydrogen Bond Donor Count
6
Hydrogen Bond Acceptor Count
6
Rotatable Bond Count
1
Heavy Atom Count
13
Complexity
155
Defined Atom Stereocenter Count
4
SMILES
C([C@@H]1[C@@H]([C@@H]([C@H](C(O1)O)N)O)O)O.Cl
InChi Key
QKPLRMLTKYXDST-BMZZJELJSA-N
InChi Code
InChI=1S/C6H13NO5.ClH/c7-3-5(10)4(9)2(1-8)12-6(3)11;/h2-6,8-11H,1,7H2;1H/t2-,3-,4+,5-,6?;/m1./s1
Chemical Name
(3R,4R,5R,6R)-3-amino-6-(hydroxymethyl)oxane-2,4,5-triol;hydrochloride
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

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
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 : ~100 mg/mL (~463.76 mM)
DMSO : ~25 mg/mL (~115.94 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (11.59 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (11.59 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (11.59 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


Solubility in Formulation 4: 100 mg/mL (463.76 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 4.6376 mL 23.1879 mL 46.3757 mL
5 mM 0.9275 mL 4.6376 mL 9.2751 mL
10 mM 0.4638 mL 2.3188 mL 4.6376 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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In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
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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.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
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