5-Aminolevulinic acid 78mg/g gel
Requires a prescription from a doctor or prescriber
A compound produced from succinyl-CoA and glycine as an intermediate in heme synthesis.
Safety information for pregnancy and breastfeeding
Pregnancy
No carcinogenicity testing has been carried out using ALA.
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
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MHRA alerts for Aminolevulinic acid hydrochloride
Safety monitoring data
Yellow Card reports
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1 branded products available
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Ameluz 78mg/g gel
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Supply & safety information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0.
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 7 · Randomised trials: 6 · 1972–2026
Showing the 50 most relevant studies, sorted by most relevant.
Tian Y, Yao Y, Zhang J
2026
- Photochemotherapy
- Keratosis, Actinic
- Imiquimod
Actinic keratosis is a common precancerous epidermal skin lesion characterized by rough, scaly patches on sun-exposed areas due to chronic UV exposure, and it carries a risk of progressing to squamous cell carcinoma. Both photodynamic therapy and imiquimod cream have been proven to be effective therapeutic option for actinic keratosis. However, there is no comprehensive systematic review that compare the efficacy of the two treatments. We conducted a comprehensive search of literature to evaluate the efficacy of photodynamic therapy and imiquimod cream in treating actinic keratosis. Meta-analysis was performed using Review Manager 5.4 software. After the screening of 1144 studies and 11 reports, six randomized controlled trials with two evaluation indicators were included. Our meta-analysis indicated that photodynamic therapy, particularly 5-aminolevulinic acid photodynamic therapy, produced superior results than imiquimod cream when analysing the lesion clearance rate, and imiquimod treatment is more likely to cause adverse reactions such as ulceration/crusting compared to photodynamic therapy.
Abstract licence: CC BY-NC-ND
Ontario health technology assessment series, 2020
- Glioma
- Brain Neoplasms
- Aminolevulinic Acid
Kuryata O, Akimov O, Riabushko M, et al.
2024
5-Aminolevulinic acid (5-ALA) is an essential compound in the biosynthesis of heme, playing a critical role in various physiological processes within the human body. This review provides the thorough analysis of the latest research on the molecular mechanisms and potential therapeutic benefits of 5-ALA in managing metabolic disorders. The ability of 5-ALA to influence immune response and inflammation, oxidative/nitrosative stress, antioxidant system, mitochondrial functions, as well as carbohydrate and lipid metabolism, is mediated by molecular mechanisms associated with the suppression of the transcription factor NF-κB signaling pathway, activation of the transcription factor Nrf2/heme oxygenase-1 (HO-1) system leading to the formation of heme-derived reaction products (carbon monoxide, ferrous iron, biliverdin, and bilirubin), which may contribute to HO-1-dependent cytoprotection through antioxidant and immunomodulatory effects. Additionally, it regulates the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha, cytochrome c oxidase subunit IV, uncoupling proteins UCP1 and UCP2, glucose transporters GLUT1 and GLUT2, and sterol regulatory element-binding protein 1c in relevant tissues. Randomized controlled trials have confirmed the effects of 5-ALA on glucose control in both prediabetic and diabetic patients, noting its safety and tolerability, as well as the safety of its combined use with oral hypoglycemic agents. Only minor side effects have been reported. However, the impact of 5-ALA on markers of systemic inflammation, oxidative and nitrosative stress, and dyslipidemia was not evaluated in these studies. At the same time, preparations of 5-ALA may potentially be effective not only in the treatment of prediabetes and type 2 diabetes mellitus (T2DM), but also in other conditions associated with systemic inflammation, oxidative or nitrosative stress, mitochondrial dysfunction, as well as disorders of carbohydrate and lipid metabolism. It has been concluded that the promising advancement of formulations containing 5-ALA may pave the way for new strategies in preventing and treating these diseases, with subsequent preclinical and clinical trials likely to follow.
Abstract licence: CC BY
R. Sumiyoshi, T. Koga, O. Kamisawa, et al.
Cureus, 2025
Objective: To evaluate the efficacy and safety of 5-aminolevulinic acid hydrochloride/sodium ferrous citrate (5-ALA-HCl/SFC) in patients with adult-onset Still’s disease (AOSD) refractory to corticosteroids. Methods/design: This multicenter, investigator-initiated, randomized, double-blind, placebo-controlled, parallel-group phase II trial was designed to enroll 30 participants but was prematurely terminated after enrolling four participants because of slow recruitment. Participants were randomized to receive 5-ALA-HCl/SFC (100 or 300 mg/day) or placebo for 8 weeks. The primary endpoint was the achievement of adapted ACR 30 at week 4. Results: All four enrolled participants achieved adapted ACR 30 at week 4. Adapted ACR 50/ 70/ 90 responses and improvements in systemic feature score, serum ferritin, and quality of life varied among individuals. No serious adverse events were observed. Conclusion: Efficacy signals were observed, especially in the high-dose group; however, the small sample size precludes definitive conclusions. Further research is required to confirm this.
Abstract licence: CC BY
Ohtake A, Abe Y, Murayama K, et al.
2025
Ohtake A, Abe Y, Murayama K, et al.
2026
- Leigh Disease
- Ferrous Compounds
- Citrates
Bozell, L. Moens, D., et al.
Resources Conservation and Recycling, 2000
D. Piacquadio, Diana M. Chen, H. F. Farber, et al.
Archives of dermatology, 2004
Jun Liang, Xiaonian Lu, Hui Tang, et al.
Photodermatology, 2009
- Photochemotherapy
- Condylomata Acuminata
- Aminolevulinic Acid
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
3.9 hours
Mechanism
According to the presumed mechanism of action, photosensitization following appl…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
50-60%
### Topical gel
Pharmacokinetics (PK) of aminolevulinic acid (ALA) and PpIX was evaluated in a trial of 12…
Half-life
3.9 hours
Protein binding
25%
Volume of distribution
2.8 L
Metabolism
6%
Elimination
12 hours
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L40343]
As a topical solution, ALA can also be used for the same indication mentioned previously in addition to AKs of the upper extremities, but in conjunction with blue light illumination using the BLU-U Blue Light Photodynamic Therapy Illuminator.
[L40348]
Finally, ALA is also available as an oral solution to be used as an adjunct for the visualization of glioma during surgery.
[L40353]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 42 of 42 interactions
[L40353]
No carcinogenicity testing has been carried out using ALA. No evidence of mutagenic effects was seen in four studies conducted with ALA to evaluate this potential.
In the Salmonella-Escherichia coli/mammalian microsome reverse mutation assay (Ames mutagenicity assay), no increases in the number of revertants were observed with any of the tester strains. In the Salmonella-Escherichia coli/mammalian microsome reverse mutation assay in the presence of solar light radiation (Ames mutagenicity assay with light), ALA did not cause an increase in the number of revertants per plate of any of the tester strains in the presence or absence of simulated solar light. In the L5178Y TK± mouse lymphoma forward mutation assay, ALA was evaluated as negative with and without metabolic activation under the study conditions.
PpIX formation was not demonstrated in any of these in vitro studies. In the in vivo mouse micronucleus assay, ALA was considered negative under the study exposure conditions. In contrast, at least one report in the literature has noted genotoxic effects in cultured rat hepatocytes after ALA exposure with PpIX formation.
Other studies have documented oxidative DNA damage in vivo and in vitro as a result of ALA exposure.
[L40348]
No assessment of effects of ALA HCl on fertility has been performed in laboratory animals. It is unknown what effects systemic exposure to ALA HCl might have on fertility or reproductive function.
[L40348]
How the body processes this drug — absorption, distribution, metabolism, and elimination
### Topical gel
Pharmacokinetics (PK) of aminolevulinic acid (ALA) and PpIX was evaluated in a trial of 12 adult subjects with mild to moderate AK with at least 10 AK lesions on the face or forehead. A single dose of one entire tube of ALA (2 grams) was applied under occlusion for 3 hours followed by photodynamic therapy (PDT) to a total area of 20 cm2. The mean ± SD baseline plasma ALA and PpIX concentrations were 20.16 ± 16.53 ng/mL and 3.27 ± 2.40 ng/mL, respectively.
In most subjects, an up to 2.5-fold increase of ALA plasma concentrations was observed during the first 3 hours after ALA application. The mean ± SD area under the concentration time curve (AUC0-t) and maximum concentration (Cmax) for baseline corrected ALA (n=12) were 142.83 ± 75.50 ng.h/mL and 27.19 ± 20.02 ng/mL, respectively. The median Tmax (time at which Cmax occurred) was 3 hours.
### Topical solution
Two human pharmacokinetic (PK) studies were conducted in subjects with minimally to moderately thick actinic keratoses on the upper extremities, having at least 6 lesions on one upper extremity and at least 12 lesions on the other upper extremity.
A single dose comprising of two topical applications of ALA topical solution (each containing 354 mg ALA HCl) were directly applied to the lesions and occluded for 3 hours prior to light treatment.
The first PK study was conducted in 29 subjects and PK parameters of ALA were assessed. The baseline corrected mean ± SD of the maximum concentration (Cmax) of ALA was 249.9 ± 694.5 ng/mL and the median Tmax was 2 hours post dose. The mean ± SD exposure to ALA, as expressed by area under the concentration time curve (AUCt) was 669.9 ± 1610 ng·hr/mL.
The mean ± SD elimination half-life (t1/2) of ALA was 5.7 ± 3.9 hours.
A second PK study was conducted in 14 subjects and PK parameters of ALA and PpIX were measured. The baseline corrected PpIX concentrations were negative in at least 50% of samples in 50% (7/14) subjects and AUC could not be estimated reliably. The baseline-corrected mean ± SD of Cmax for ALA and PpIX was 95.6 ± 120.6 ng/mL and 0.95 ± 0.71 ng/mL, respectively.
The median Tmax of ALA and PpIX was 2 hours post dose and 12 hours post dose, respectively. The mean AUCt of ALA was 261.1 ± 229.3 ng·hr/mL. The mean ± SD t1/2 of ALA was 8.5 ± 6.7 hours.
### Oral solution
In 12 healthy subjects, the absolute bioavailability of ALA following the recommended dose of ALA solution was 100.0% + 1.1 with a range of 78.5% to 131.2%.
Maximum ALA plasma
concentrations were reached with a median of 0.8 hour (range 0.5 – 1.0 hour).
[L40348][L40353]
In another pharmacokinetic studies with 6 healthy volunteers using a 128 mg dose, the mean half-life was 0.70 ± 0.18 h after the oral dose and 0.83 ± 0.05 h after the intravenous dose.
[L48491]
[L40353]
[L40353]
[L40353]
Proteins and enzymes this drug interacts with in the body
Proteins that transport this drug across cell membranes
PMID:15521010 PMID:18367661 PMID:19685173 PMID:26320580 PMID:7896779 PMID:8914574 PMID:9835627
Primarily responsible for the absorption of dietary di- and tripeptides from the small intestinal lumen (By similarity). Mediates transepithelial transport of muramyl and N-formylated bacterial dipeptides contributing to recognition of pathogenic bacteria by the mucosal immune system PMID:15521010 PMID:9835627
PMID:16434549 PMID:18367661 PMID:7756356
Transports neutral and anionic dipeptides with a proton to peptide stoichiometry of 2:1 or 3:1 (By similarity). In kidney, involved in the absorption of circulating di- and tripeptides from the glomerular filtrate .
PMID:7756356
Can also transport beta-lactam antibiotics, such as the aminocephalosporin cefadroxil, and other antiviral and anticancer drugs .
PMID:16434549
Transports the dipeptide-like aminopeptidase inhibitor bestatin (By similarity). Also able to transport carnosine .
PMID:31073693
Involved in innate immunity by promoting the detection of microbial pathogens by NOD-like receptors (NLRs) (By similarity).
Mediates transport of bacterial peptidoglycans across the plasma membrane or, in macrophages, the phagosome membrane: catalyzes the transport of certain bacterial peptidoglycans, such as muramyl dipeptide (MDP), the NOD2 ligand PMID:20406817
Involved compounds
Involved compounds
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Involved compounds
Involved compounds
ATC L01XD04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Aminolevulinic acid
Matched from: Aminolevulinic acid hydrochloride
Additional database identifiers
Drugs Product Database (DPD)
12216
ChemSpider
134
BindingDB
50240386
PDB
FVT
ZINC
ZINC000003782550
HUGO Gene Nomenclature Committee (HGNC)
HGNC:395
GenAtlas
ALAD
GeneCards
ALAD
GenBank Gene Database
M13928
GenBank Protein Database
178329
UniProt Accession
HEM2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9280
GeneCards
PPOX
UniProt Accession
PPOX_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10920
GenAtlas
SLC15A1
GeneCards
SLC15A1
GenBank Gene Database
U13173
GenBank Protein Database
773588
Guide to Pharmacology
984
UniProt Accession
S15A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10921
GenAtlas
SLC15A2
GeneCards
SLC15A2
GenBank Gene Database
S78203
GenBank Protein Database
999213
Guide to Pharmacology
985
UniProt Accession
S15A2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72