Transtorine demonstrates growth inhibitory efficacy with MIC values of 0.38, 0.5, and 0.45 mg/mL against Pseudomonas aeruginosa, Enterobacter cloacae, and Staphylococcus aureus, respectively[1].

Metabolism / Metabolites
Uremic toxins often accumulate in the blood due to overeating or poor kidney filtration. Most uremic toxins are metabolic waste products that are normally excreted through urine or feces.

[1]. Transtorine, a new quinoline alkaloid from Ephedra transitoria. J Nat Prod. 1998 Feb;61(2):262-3.

Kynuric acid is a quinoline monocarboxylic acid, specifically quinoline-2-carboxylic acid with a hydroxyl group substituted at the C-4 position. It has multiple functions, including acting as a G protein-coupled receptor agonist, NMDA receptor antagonist, nicotine receptor antagonist, neuroprotective agent, human metabolite, and a Saccharomyces cerevisiae metabolite. It is a monohydroxyquinoline and quinoline monocarboxylic acid, and is also the conjugate acid of kynuric acid. Kynuric acid is currently being investigated in the clinical trial NCT02340325 (FS2 Safety and Tolerability Study in Healthy Volunteers). Kynuric acid has been reported to be present in ephedra, Ephedra sinica, and other organisms with relevant data. Kynuric acid is a uremic toxin. Based on chemical and physical properties, uremic toxins can be classified into three main categories: 1) small, water-soluble, non-protein-bound compounds, such as urea; 2) small, lipid-soluble and/or protein-bound compounds, such as phenols; and 3) larger, so-called medium-molecular-weight compounds, such as β2-microglobulin. Long-term exposure to uremic toxins can lead to various diseases, including kidney damage, chronic kidney disease, and cardiovascular disease. Kynuronic acid (KYNA) is a known antagonist of endogenous glutamate ionotropic excitatory amino acid receptors (such as N-methyl-D-aspartate (NMDA) receptors, α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors, and phycocyanine receptors) and nicotinic cholinergic subtype α7 receptors. In animal models of neurodegenerative diseases, KYNA has been shown to possess neuroprotective and anticonvulsant activities. Due to its neuromodulatory properties, KYNA is hypothesized to be involved in the pathogenesis of various neurological diseases, including those related to aging. Abnormal patterns of KYNA metabolism at different stages in the central nervous system (CNS) have been reported in Alzheimer's disease, Parkinson's disease, and Huntington's disease. KYNA metabolism is significantly elevated in HIV-1 infected individuals and Lyme disease patients with neurological infections. During aging, KYNA metabolism in the rat CNS exhibits a characteristic pattern of changes throughout the lifespan. Prenatal KYNA levels are significantly elevated, followed by a sharp decline on the day of birth. Kynuronic acid (KYNA) exhibits low activity during individual development, slowly and gradually increasing during maturation and aging. This significant pattern of altered KYNA metabolism in the mammalian brain is thought to stem from tissue development of neuronal connections and synaptic plasticity, development of receptor recognition sites, and maturation and aging processes. There is substantial evidence that kynuronic acid can improve cognition and memory, but other studies suggest it can interfere with working memory. Cognitive impairment in various neurodegenerative diseases is accompanied by significant decreases and/or increases in KYNA metabolism. Increased KYNA metabolism in Alzheimer's disease and Down syndrome, as well as enhanced KYNA function in the early stages of Huntington's disease, support the idea that elevated central nervous system KYNA levels may be a potential mechanism for cognitive decline. Kynuronic acid is the only known endogenous N-methyl-D-aspartate (NMDA) receptor antagonist that mediates glutamatergic dysfunction. Schizophrenia is a dopaminergic neurotransmission disorder, but glutamatergic neurotransmission appears to play a crucial role in the regulation of the dopaminergic system. Although kynurenic acid has NMDA receptor antagonistic effects, low doses of kynurenic acid can also block nicotinic acetylcholine receptors, meaning that elevated kynurenic acid levels can explain psychotic symptoms and cognitive decline. Studies have shown that patients with schizophrenia have higher levels of kynurenic acid in the cerebrospinal fluid and key central nervous system regions compared to controls (A3279, A3280). Kynurenic acid is a metabolite of Saccharomyces cerevisiae, produced by or present in the yeast. It is a broad-spectrum excitatory amino acid antagonist and is frequently used as a research tool.

C10H7NO3

189.17

189.043

13593-94-7

3845

White to off-white solid powder

1.429g/cm3

358.4ºC at 760mmHg

280 °C

170.5ºC

1.226

2

4

1

14

309

0

HCZHHEIFKROPDY-UHFFFAOYSA-N

InChI=1S/C10H7NO3/c12-9-5-8(10(13)14)11-7-4-2-1-3-6(7)9/h1-5H,(H,11,12)(H,13,14)

4-oxo-1H-quinoline-2-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)