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5-Aminolevulinic acid HCl

Cat.No.S2553

5-Aminolevulinic Acid HCl(5-ALA hydrochloride) is an intermediate in the porphyrin synthesis pathway, used as a photosensitizing agent and a antineoplastic agent.
5-Aminolevulinic acid HCl Chemical Structure

Chemical Structure

Molecular Weight: 167.59

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 167.59 Formula

C5H9NO3.HCl

Storage (From the date of receipt)
CAS No. 5451-09-2 Download SDF Storage of Stock Solutions

Synonyms 5-ALA hydrochloride Smiles C(CC(=O)O)C(=O)CN.Cl

Solubility

In vitro
Batch:

DMSO : 34 mg/mL (202.87 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : 34 mg/mL

Ethanol : 10 mg/mL

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid 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 master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

In vitro

5-aminolevulinic acid (5-ALA)-Photodynamic therapy (PDT) results in down regulation of nuclear factor kappa B (NFkappaB) and baculovirus inhibitor-of-apoptosis repeat containing-3 (BIRC-3) protein. 5-aminolevulinic acid (5-ALA)-Photodynamic therapy (PDT) causes increase in Bax:Bcl-2 ratio and mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF). [1] 5-aminolevulinic acid yields reactive oxygen species upon metal-catalyzed oxidation and causes in vivo and in vitro impairment of rat liver mitochondria and DNA damage. 5-aminolevulinic acid induces a dose-dependent damage in nuclear and mitochondrial DNA in human SVNF fibroblasts and rat PC12 cells. [2] 5-aminolevulinic acid dose-dependently decreases cAMP levels (maximal inhibition of 38%, at 1 mM), due to an inhibition of basaladenylate cyclase activity. 5-aminolevulinic acid also inhibits fluoride- and Gpp(NH)p-stimulated, but not the forskolin-stimulated adenylate cyclase activity. 5-aminolevulinic acid also inhibits the activity of adenylate cyclase in membranes isolated from rat cortex and striatum and from human cortex. [3] 5-aminolevulinic acid (0-3mM) dose-dependently inhibits glutamate uptake by astrocyte cultures. 5-aminolevulinic acid significantly reduces both the K(m) and V(max) of glutamate uptake indicating an uncompetitive inhibition. 5-aminolevulinic acid significantly increases astrocyte lipoperoxidation in astrocytes incubated under these conditions. [4] 5-aminolevulinic acid mediated sonodynamic therapy exhibits synergistic apoptotic effects on THP-1 macrophages, involving excessive intracellular reactive oxygen species generation and MMP loss. [5]

References
  • [4] https://pubmed.ncbi.nlm.nih.gov/9990306/
  • [5] https://pubmed.ncbi.nlm.nih.gov/23426386/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT04626661 Completed
Mitochondrial Oxygenation Measurement|Measurement Error|Healthy
Sanquin-LUMC J.J van Rood Center for Clinical Transfusion Research|Leiden University Medical Center
June 15 2020 --
NCT00241670 Completed
Brain Cancer|Brain Tumors|Cancer of Brain|Primary Brain Tumors|Brain Tumor Primary
medac GmbH
October 1999 Phase 3

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