THIOSULFURIC ACID

First marketed in 1921

Details

Stereochemistry	ACHIRAL
Molecular Formula	H2O3S2
Molecular Weight	114.144
Optical Activity	NONE
Defined Stereocenters	0 / 0
E/Z Centers	0
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

OS(O)(=O)=S

InChI

InChIKey=DHCDFWKWKRSZHF-UHFFFAOYSA-N

InChI=1S/H2O3S2/c1-5(2,3)4/h(H2,1,2,3,4)

HIDE SMILES / InChI

Molecular Formula	H2O3S2
Molecular Weight	114.144
Charge	0
Count

Stereochemistry	ACHIRAL
Additional Stereochemistry	No
Defined Stereocenters	0 / 0
E/Z Centers	0
Optical Activity	NONE

Description
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/201444s000lbl.pdf | https://www.ncbi.nlm.nih.gov/pubmed/26742969 | https://www.ncbi.nlm.nih.gov/pubmed/28825580

Sodium thiosulfate (sodium thiosulphate/STS) is a chemical and medication. As a medication, it is used in combination with sodium nitrite under the trade name to NITHIODOTE treat cyanide poisoning. The primary route of endogenous cyanide detoxification is by enzymatic transulfuration to thiocyanate (SCN- ), which is relatively nontoxic and readily excreted in the urine. Sodium thiosulfate is thought to serve as a sulfur donor in the reaction catalyzed by the enzyme rhodanese, thus enhancing the endogenous detoxification of cyanide. In addition, Sodium thiosulfate is used in calciphylaxis in hemodialysis patients with end-stage kidney disease. Calciphylaxis is vasculopathy characterized by ischemia and painful skin necrosis due to calcification and intimal fibroplasia of thrombosis of the panicular arterioles. Sodium thiosulfate is used as treatment due to its antioxidant activity and as a chelating. Sodium thiosulfate renders renal protection by modulating the mitochondrial KATP channel for preventing urolithiasis. Moreover, STS was assumed to play a vital role in on ischemia reperfusion injury (IR). The effectiveness of STS as a cardioprotective agent was attributed to the reduction of apoptosis by binding to the active site of caspase-3 in silico, which was substantiated by the reduced expression of caspase-3 and poly ADP ribose polymerase levels.

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
Caspase-3 21 Target ID: P42574 Gene ID: 836.0 Gene Symbol: CASP3 Target Organism: Homo sapiens (Human) Sources: https://www.ncbi.nlm.nih.gov/pubmed/28965151	Binding Agent 1076
ATP-sensitive inward rectifier potassium channel 8 9 Target ID: Q15842 Gene ID: 3764.0 Gene Symbol: KCNJ8 Target Organism: Homo sapiens (Human) Sources: https://www.ncbi.nlm.nih.gov/pubmed/26742969	Modulator 846
ATP-sensitive inward rectifier potassium channel 11 10 Target ID: Q14654 Gene ID: 3767.0 Gene Symbol: KCNJ11 Target Organism: Homo sapiens (Human) Sources: https://www.ncbi.nlm.nih.gov/pubmed/26742969	Modulator 846

Conditions

Condition	Modality	Highest Phase	Product
Acute cyanide poisoning 9 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/201444s000lbl.pdf	Curative	Approved 8583	NITHIODOTE Approved Use Sodium nitrite and sodium thiosulfate are indicated for sequential use for treatment of acute cyanide poisoning that is judged to be lifethreatening. Use with caution if the diagnosis of cyanide poisoning is uncertain. Launch Date 2011
Calciphylaxis 7 Sources: https://www.ncbi.nlm.nih.gov/pubmed/28825580	Palliative	Phase III 665	Unknown Approved Use Unknown
Nephrolithiasis 23 Sources: https://www.ncbi.nlm.nih.gov/pubmed/19369406	Preventing	Not Provided 511	Unknown Approved Use Unknown

PubMed

Title	Date	PubMed
Gestational urinary hyperthiosulfaturia protects hypercalciuric normal pregnant women from nephrolithiasis.	2004	15783122
Bactericidal activities of commonly used antiseptics against multidrug-resistant mycobacterium tuberculosis.	2002	12011515
Creation of transdermal pathways for macromolecule transport by skin electroporation and a low toxicity, pathway-enlarging molecule.	1999-10	10619443
Nutritional aspects of dissimilatory sulfate reduction in the human large intestine.	1997-11	9462959
Bactericidal activities of povidone-iodine against Mycobacterium.	1997	9403266
The utilization of thiocyanate as a nitrogen source by a heterotrophic bacterium: the degradative pathway involves formation of ammonia and tetrathionate.	1994-10	8000536
Application of new fluorescent thiol reagent to diagnosis of homocystinuria.	1991-10-26	1681358
Determination of thiosulfate in body fluids by GC and GC/MS.	1991-05-01	1943059
A rapid and accurate spectrofluorometric method for quantification and screening of urinary porphyrins.	1988-02	3342508
Sodium thiosulfate disposition in humans: relation to sodium nitroprusside toxicity.	1983-01	6600205
Selective vs. nonselective media and direct plating vs. enrichment technique in isolation of Vibrio cholerae: recommendations for clinical laboratories.	1980-09	7003031
Sucrose teepol tellurite agar: a new selective indicator medium for isolation of Vibrio species.	1977-04	856920
METABOLISM, TOXICITY AND MANNER OF ACTION OF GOLD COMPOUNDS USED IN THE TREATMENT OF ARTHRITIS. I. HUMAN PLASMA AND SYNOVIAL FLUID CONCENTRATION AND URINARY EXCRETION OF GOLD DURING AND FOLLOWING TREATMENT WITH GOLD SODIUM THIOMALATE, GOLD SODIUM THIOSULFATE, AND COLLOIDAL GOLD SULFIDE.	1941-07	16694848

Patents

Sample Use Guides

In Vivo Use Guide

acute cyanide intoxication: Adults: 1.) Sodium Nitrite -10 mL of a 3% solution (300 mg) of sodium nitrite at the rate of 2.5 to 5 mL/minute 2.) Sodium Thiosulfate - 50 mL of a 25% solution (12.5 g) of a sodium thiosulfate solution immediately following administration of sodium nitrite. Children: 1.) Sodium Nitrite -0.2 mL/kg of a 3% solution (6 mg/kg or 6-8 mL/m2 BSA) of sodium nitrite at the rate of 2.5 to 5 mL/minute not to exceed 10 mL (300 mg) 2.) Sodium Thiosulfate - 1 mL/kg of body weight using a 25% solution (250 mg/kg or approximately 30-40 mL/m2 of BSA) not to exceed 50 mL (12.5 g) total dose immediately following administration of sodium nitrite.

Route of Administration: Intravenous

In Vitro Use Guide

There were investigated the effectiveness of Sodium thiosulfate (STS) as a cardioprotective agent is attributed to the reduction of apoptosis by binding to the active site of caspase-3 in silico, which was substantiated by the reduced expression of caspase-3 and poly ADP ribose polymerase levels. STS of 1 mM recovered H9C2 cells from glucose oxidase/catalase-induced apoptosis. The isolated rat heart treated with STS prior to reperfusion injury (IR) injury improved its hemodynamics and reduced the infarct size to 9%. An in silico docking analysis revealed higher binding affinity of STS for caspase-3 with a binding energy of - 60.523 kcal/mol for the complex.

Substance Class	Chemical Created by `admin` on `Mon Mar 31 18:47:45 GMT 2025` Edited by `admin` on `Mon Mar 31 18:47:45 GMT 2025`
Record UNII	7K79Y2EKKP
Record Status	`Validated (UNII)`
Record Version

Download

Name

Type

Language

THIOSULFURIC ACID

Systematic Name

English

THIOSULFURIC ACID (H2S2O3)

Preferred Name

English

MONOSULFANEMONOSULFONIC ACID

Systematic Name

English

Classification Tree Code System Code

WHO-ATC

V03AB06