Accession Number

Aurothioglucose, also known as gold thioglucose, was formerly used to treat rheumatoid arthritis.

Contemporary research on the effect of gold salts treatment began in 1935, primarily to reduce inflammation and to slow disease progression in patients with rheumatoid arthritis 2. The use of gold compounds has decreased since the 1980s owing to numerous side effects, limited efficacy, and slow onset of action. Many if not most gold compounds that were indicated for rheumatoid arthritis therapy have since been replaced with the use of various current disease modifying anti-rheumatic drugs (DMARDs) like methotrexate and others, which are far more effective.

Small Molecule
Approved, Withdrawn
Average: 392.18
Monoisotopic: 391.999289
Chemical Formula
  • Auromyose
  • Aurothioglucose
  • Gold thioglucose



Aurothioglucose is indicated for the adjunctive treatment of early active adult and juvenile type rheumatoid arthritis that is not adequately controlled by other anti-inflammatory agents and conservative measures like salicylate, glucocorticoids, etc. 5,6. In chronic, advanced cases of rheumatoid arthritis, such gold therapy is not demonstrated to be as valuable 6.

Antirheumatic measures such as salicylate and other anti-inflammatory drugs (both steroidal and non steroidal) may be continued after initiation of gold therapy 6. After improvement commences, these measures may be discontinued slowly as symptoms permit 6.

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After administration, patient serum levels of gold rise sharply but decline over the following week 6. Peak levels with aqueous preparations are higher and decline faster than those with oily preparations 6. Regular weekly administration produces a continuous rise in the basal value for several months, after which the serum level becomes relatively stable 6. After a standard weekly dose, considerable individual variation in the levels of gold can be observed 6. A steady decline in gold levels occurs when the interval between injections is lengthened, and small amounts may be found in the serum for months after discontinuation of therapy 6. The incidence of toxic reactions is seemingly unrelated to the plasma level of gold, but may perhaps be more associated with the total cumulative content of gold in the body 6.

Mechanism of action

Rheumatoid arthritis is an autoimmune disease in which the body's immune system mistakenly attacks the lining of various skeletal bone joints of the body 1,9. These attacks are facilitated by various pro-inflammatory immune cells and agents like cytokines, histamines, mast cells, macrophages, monocytes, lymphocytes, leukocytes, and many others 1. The longterm result of this unwanted immune response is chronic inflammation and painful tissue damage 1,9. The cause of the malfunctioning immune system in rheumatoid arthritis is unknown and there is no definitive cure for the condition 1,9.

Similarly, the mechanism of action of aurothioglucose is also not well elucidated. Nevertheless, some studies have suggested that the combination of both the sulfhydryl ligand and aureus cation present in aurothioglucose elicits an inhibitory effect on adenylyl cyclase activity in human lymphocyte membranes and in membranes of T and B lymphocyte subsets 1. In particular, such inhibition of the activity of adenylyl cyclase and its various isoforms would theoretically also limit the cyclases' ability to induce mast cell degranulation and histamine release, to enhance respiratory burst effects, to stimulate the action of resting macrophages, to induce and activate phagocytes, to induce neutrophil chemotaxis, etc. - all of which are pro-inflammatory actions 1.

UAdenylate cyclase type 1Not AvailableHumans
UAdenylate cyclase type 2Not AvailableHumans
UAdenylate cyclase type 5Not AvailableHumans

In general, aurothioglucose is administered via intramuscular injection - preferably intragluteally 8 - after which the resultant absorption is typically slow and erratic 4.

Gold is absorbed from injection sites, reaching peak concentration in blood in about 4 to 6 hours 6. After a single intramuscular injection of 50 mg of aurothioglucose suspension in two subjects, peak serum levels were observed at approximately 235 g/dL and 450 g/dL 6.

Storage of gold in human tissues depends upon organ mass as well as the concentration of gold 6.Subsequently, tissues having the highest gold levels (w/w) may not necessarily have the largest total amounts of gold 6. The highest concentrations of gold are generally found in the lymph nodes, adrenal glands, liver, kidneys, bone marrow, and spleen 6. Relatively small concentrations are actually found in the articular structures 6. In particular, following the administration of aurothioglucose doses, about 85% of the resultant plasma gold will be stored in the major bodily gold depots, which in decreasing order of total gold content are, the lymph nodes, bone marrow, liver, skin, and bone 6,8.

Volume of distribution

Readily accessible data regarding the volume of distribution of aurothioglucose is not available.

Protein binding

In plasma, 95-99% of the drug is bound to albumin fraction 5,3.


Although the exact metabolic fate of aurothioglucose is not formally understood, the principal gold species that can be found in the urine and blood of a patient following the administration of the drug is [Au(CN)2]- 5.

Route of elimination

Following a single intramuscular injection of 50 mg aurothioglucose in each of two patients, one study determined that approximately 70% of the agent is eliminated in the urine and 30% in the faeces 5. In general, excretion is primarily in the urine 3.


The biological half-life of gold salts (like aurothioglucose) following a single 50 mg dose demonstrates a biological half-life of about 3-27 days, where the half-life seemingly increases with increased number of doses 3. Following successive weekly doses, the half-life increases and may become 14-40 days after the third dose and up to 168 days after the eleventh weekly dose 5.


When a standard weekly treatment schedule of aurothioglucose administrations is followed, about 40% of the given dose is excreted each week, while the remainder is excreted over a longer period 6.

Adverse Effects
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Overdose as a result of too rapid increases in dosing with aurothioglucose will be manifested by rapid appearance of toxic reactions, including those that are particular to renal damage, like hematuria and proteinuria, while hematologic effects include thrombocytopenia and granulocytopenia 6.

Other toxic effects, including fever, nausea, vomiting, diarrhea, and various skin disorders like papulovesicular lesions, urticaria, and exfoliative dermatitis, each of which are typically combined with severe pruritus can also develop 6.

The intramuscular TDLo for males is reported to be approximately 3.357 mg/kg when considering sense organs and special senses like eye vision and about 5.5 mg/kg for affects on the lungs, thorax, or respiration 7. For women, the intramuscular TDLo for effects on the liver, gastrointestinal tract, and cholestatic jaundice is between 2.6-2.7 mg/kg while the value for effects on the kidney, ureter, bladder, and acute renal failure, acute tubular necrosis, and other changes in urine composition is about 14.402 mg/kg 7.

Affected organisms
  • Humans and other mammals
Not Available
Pharmacogenomic Effects/ADRs
Not Available


Drug Interactions
This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
AbacavirAbacavir may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
AcarboseAcarbose may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
AceclofenacAceclofenac may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
AcemetacinAcemetacin may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
AcetaminophenAcetaminophen may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
AcetazolamideAcetazolamide may increase the excretion rate of Aurothioglucose which could result in a lower serum level and potentially a reduction in efficacy.
Acetylsalicylic acidAcetylsalicylic acid may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
AclidiniumAclidinium may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
AcrivastineAurothioglucose may decrease the excretion rate of Acrivastine which could result in a higher serum level.
AcyclovirAcyclovir may decrease the excretion rate of Aurothioglucose which could result in a higher serum level.
Additional Data Available
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Food Interactions
Not Available


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International/Other Brands
Brenol / Oronol / Romosol / Solganal / Solganal B
Brand Name Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImage
Solganal Inj 50mg/mlSuspensionIntramuscularSchering Plough1940-12-312003-07-14Canada flag
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ATC Codes
M01CB04 — Aurothioglucose
Drug Categories
Chemical TaxonomyProvided by Classyfire
This compound belongs to the class of organic compounds known as hexoses. These are monosaccharides in which the sugar unit is a is a six-carbon containing moeity.
Organic compounds
Super Class
Organic oxygen compounds
Organooxygen compounds
Sub Class
Carbohydrates and carbohydrate conjugates
Direct Parent
Alternative Parents
Oxanes / Secondary alcohols / Polyols / Oxacyclic compounds / Organic transition metal salts / Primary alcohols / Organosulfur compounds / Organic zwitterions / Hydrocarbon derivatives
Alcohol / Aliphatic heteromonocyclic compound / Hexose monosaccharide / Hydrocarbon derivative / Organic salt / Organic transition metal salt / Organic zwitterion / Organoheterocyclic compound / Organosulfur compound / Oxacycle
Molecular Framework
Aliphatic heteromonocyclic compounds
External Descriptors
oxanes (CHEBI:2930)

Chemical Identifiers

CAS number
InChI Key


General References
  1. Botz B, Bolcskei K, Kereskai L, Kovacs M, Nemeth T, Szigeti K, Horvath I, Mathe D, Kovacs N, Hashimoto H, Reglodi D, Szolcsanyi J, Pinter E, Mocsai A, Helyes Z: Differential regulatory role of pituitary adenylate cyclase-activating polypeptide in the serum-transfer arthritis model. Arthritis Rheumatol. 2014 Oct;66(10):2739-50. doi: 10.1002/art.38772. [PubMed:25048575]
  2. Shaw III CF: Gold-based therapeutic agents. Chem Rev. 1999 Sep 8;99(9):2589-600. [PubMed:11749494]
  3. Arthur H. Jeske (2017). Mosby's Dental Drug Reference - E-Book (pp. 120-122). Elsevier Health Sciences. [ISBN:9780323511216]
  4. Ronald I. Shorr (2007). Drugs for the Geriatric Patient . Elsevier Health Sciences. [ISBN:9781437710359]
  5. NLM Toxnet Toxicology Data Network: Aurothioglucose [Link]
  6. RXmed: Solganal (Aurothioglucose) Monograph [Link]
  7. ChemIDplus: Aurothioglucose [USP] [Link]
  8. ScienceDirect: Aurothioglucose [Link]
  9. Arthritis Society: Rheumatoid Arthritis [Link]
KEGG Compound
PubChem Compound
PubChem Substance
Download (118 KB)

Clinical Trials

Clinical Trials


Not Available
Not Available
Dosage Forms
Not Available
Not Available


Experimental Properties
Not Available
Predicted Properties
Water Solubility96.4 mg/mLALOGPS
pKa (Strongest Acidic)12.51ChemAxon
pKa (Strongest Basic)-3ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count5ChemAxon
Hydrogen Donor Count4ChemAxon
Polar Surface Area90.15 Å2ChemAxon
Rotatable Bond Count2ChemAxon
Refractivity41.25 m3·mol-1ChemAxon
Polarizability19.88 Å3ChemAxon
Number of Rings1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterNoChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Predicted ADMET Features
Not Available


Mass Spec (NIST)
Not Available
SpectrumSpectrum TypeSplash Key
Predicted GC-MS Spectrum - GC-MSPredicted GC-MSNot Available


Pharmacological action
General Function
Metal ion binding
Specific Function
Catalyzes the formation of the signaling molecule cAMP in response to G-protein signaling. Mediates responses to increased cellular Ca(2+)/calmodulin levels (By similarity). May be involved in regu...
Gene Name
Uniprot ID
Uniprot Name
Adenylate cyclase type 1
Molecular Weight
123438.85 Da
  1. NLM Toxnet Toxicology Data Network: Aurothioglucose [Link]
Pharmacological action
General Function
Protein heterodimerization activity
Specific Function
Catalyzes the formation of the signaling molecule cAMP in response to G-protein signaling (PubMed:15385642). Down-stream signaling cascades mediate changes in gene expression patterns and lead to i...
Gene Name
Uniprot ID
Uniprot Name
Adenylate cyclase type 2
Molecular Weight
123602.25 Da
  1. NLM Toxnet Toxicology Data Network: Aurothioglucose [Link]
Pharmacological action
General Function
Protein heterodimerization activity
Specific Function
Catalyzes the formation of the signaling molecule cAMP in response to G-protein signaling (PubMed:15385642, PubMed:26206488, PubMed:24700542). Mediates signaling downstream of ADRB1 (PubMed:2470054...
Gene Name
Uniprot ID
Uniprot Name
Adenylate cyclase type 5
Molecular Weight
138906.37 Da
  1. NLM Toxnet Toxicology Data Network: Aurothioglucose [Link]

Drug created on September 22, 2015 15:48 / Updated on June 12, 2020 10:52

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