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Sodium stibogluconate
Sodium stibogluconate
Sodium stibogluconate
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Sodium stibogluconate
Clinical data
Trade namesPentostam, Stiboson, others[1]
AHFS/Drugs.comInternational Drug Names
Routes of
administration		intravenous, intramusclar[2]
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Identifiers
  • 2,4:2',4'-O-(oxydistibylidyne)bis[D-gluconic acid]
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
NIAID ChemDB
CompTox Dashboard (EPA)
ECHA InfoCard100.170.909 Edit this at Wikidata
Chemical and physical data
FormulaC12H38Na3O26Sb2
Molar mass910.899 g·mol−1
3D model (JSmol)
  • [Na+].[Na+].[Na+].O=[Sb]2(O[Sb]1(=O)OC([C@H](O)CO)[C@H](O)[C@@H](O1)C([O-])=O)O[C@@H]([C@H](O)[C@@H](O2)C([O-])=O)[C@H](O)CO
  • InChI=1S/2C6H10O7.3Na.3O.2Sb/c2*7-1-2(8)3(9)4(10)5(11)6(12)13;;;;;;;;/h2*2-5,7-8,10H,1H2,(H,12,13);;;;;;;;/q2*-2;3*+1;;;;2*+2/p-2/t2-,3?,4+,5-;2-,3-,4+,5-;;;;;;;;/m11......../s1 checkY
  • Key:RTLKTTNTVTVWPV-UQCYVGCHSA-L checkY
 ☒NcheckY (what is this?)  (verify)

Sodium stibogluconate, sold under the brand name Pentostam among others, is a medication used to treat leishmaniasis.[3] This includes leishmaniasis of the cutaneous, visceral, and mucosal types.[4] Some combination of miltefosine, paromomycin and liposomal amphotericin B, however, may be recommended due to issues with resistance.[2][5] It is given by injection.[6]

Side effects are common and include loss of appetite, nausea, muscle pains, headache, and feeling tired.[2][5] Serious side effect may include an irregular heartbeat or pancreatitis.[5] Sodium stibogluconate is less safe than some other options during pregnancy.[2] It is not believed to result in any problems if used during breastfeeding.[7] Sodium stibogluconate is in the pentavalent antimonials class of medication.[5]

Sodium stibogluconate has been studied as early as 1937 and has been in medical use since the 1940s.[8][9] It is on the World Health Organization's List of Essential Medicines.[10]

Side effects

[edit]

Sodium stibogluconate is exceedingly toxic to veins. One of the practical problems is that after a few doses it can become exceedingly difficult to find a vein in which to inject the drug. The insertion of a peripherally inserted central catheter (PICC) does not prevent the problem and can instead exacerbate it: the entire vein along the course of the PICC line can become inflamed and thrombose. Large doses of sodium stibogluconate are often administered as dilute solutions.[citation needed]

Pancreatitis is a common deleterious effect of the drug, and the serum amylase or lipase should be monitored twice weekly; there is no need to stop treatment if the amylase remains less than four times the upper limit of normal; if the amylase rises above the cut-off, then treatment should be interrupted until the amylase falls to less than twice the upper limit of normal, whereupon treatment can be resumed. Cardiac conduction disturbances are less common, but electrocardiograph (ECG) monitoring while the medicine is injected is advisable and changes quickly reverse after the drug is stopped or the infusion rate is decreased.[citation needed]

The drug can be given intramuscularly but is exceedingly painful when given by this route. It can also be given intralesionally when treating cutaneous leishmaniasis (i.e., injected directly into the area of infected skin) and again, this is exceedingly painful and does not give results superior to intravenous administration.[citation needed]

Sodium stibogluconate can also cause a reduced appetite, metallic taste in mouth, nausea, vomiting, diarrhoea, headache, tiredness, joint pains, muscle aches, dizziness, and anaphylaxis.[citation needed]

Dosing

[edit]

As dosage regimens for treating leishmaniasis have evolved, the daily dose of antimony and the duration of therapy have been progressively increased to combat unresponsiveness to therapy. In the 1980s, the use of 20 mg/kg/day (instead of 10 mg/kg/day) of antimony was recommended, but only to a maximum daily dose of 850 mg. Recent research has suggested on the basis of recent efficacy and toxicity data that this 850-mg restriction should be removed. The evidence to date, which is in their research, suggests that a regimen of 20 mg/kg/day of pentavalent antimony, without an upper limit on the daily dose, is more efficacious and is not substantially more toxic than regimens with lower daily doses. It is recommend treating all forms of leishmaniasis with a full 20 mg/kg/day of pentavalent antimony. Treatment of cutaneous leishmaniasis usually lasts for 20 days and visceral and mucosal leishmaniasis for 28 days.[11]

The dose of sodium stibogluconate is by slow intravenous infusion (at least five minutes with cardiac monitoring). The injection are stopped if there is coughing or central chest pain. The chemotherapeutic index was established by Leonard Goodwin during the Second World War when a treatment was urgently required for Allied troops during the invasion of Sicily.[12]

The duration of treatment is usually 10 to 21 days and depends on the species of Leishmania and the type of infection (cutaneous or visceral).[citation needed]

Chemical structure

[edit]

The chemical structure of sodium stibogluconate is somewhat ambiguous, and the structure shown above is idealized. Its solutions may contain multiple antimony compounds, although this heterogeneity may be unimportant. It has been speculated that the active species contains only a single antimony centre.[13]

Pharmacokinetics

[edit]

Pentavalent antimony does not appear to accumulate in the body and is excreted by the kidneys.[14]

Mechanism of action

[edit]

The mechanism of sodium stibogluconate is poorly understood, but is thought to stem from the inhibition of macromolecular synthesis via a reduction in available ATP and GTP, likely secondary to inhibition of the citric acid cycle and glycolysis. Bermann et al. studied the effects of stibogluconate on Leishmania mexicana and demonstrated a 56–65% reduction in incorporation of a label into purine nucleoside triphosphates (ATP and GTP) as well as between a 34–60% increase of label incorporation into purine nucleoside mono- and diphosphates (AMP, GMP, ADP, and GDP) following 4 hour exposure to stibogluconate.[15]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Sodium stibogluconate

View on Grokipedia
from Grokipedia
Sodium stibogluconate is a pentavalent antimonial , chemically a complex of (V) with (molecular formula approximately C₁₂H₃₆Na₃O₂₆Sb₂), used as an antiprotozoal medication primarily for treating various forms of caused by parasites. Introduced in , it has served as a first-line for over 70 years, particularly for cutaneous, mucocutaneous, and , with historical cure rates reaching 90–97% in susceptible populations. Its mechanism involves intracellular bioreduction to trivalent (Sb(III)), which inhibits the parasite's trypanothione reductase enzyme, disrupts thiol-redox homeostasis, and interferes with DNA topoisomerase I, leading to parasite death. Administered via intravenous or at a dose of 20 mg of pentavalent per kg body weight daily for 20–28 days depending on the disease form, sodium stibogluconate is not orally bioavailable and requires parenteral delivery. In the United States, it is not commercially available or FDA-approved; production was discontinued in 2020, and supplies through the Centers for Disease Control and Prevention are depleted as of 2025. It remains accessible in some endemic regions under generic names. Despite its efficacy, resistance has emerged, notably in where failure rates exceeded 65% by the late 1990s, prompting combination therapies such as with for in . Common adverse effects include injection-site pain, nausea, and fever, with serious risks encompassing (e.g., QT prolongation), , , and , necessitating ECG and biochemical monitoring during treatment. Recent advancements focus on improving its profile through liposomal formulations, cyclodextrin complexes, and nanoparticle delivery systems to enhance targeting, reduce , and overcome resistance in Leishmania donovani and other species.

Medical uses

Indications

Sodium stibogluconate is primarily indicated for the treatment of all forms of , including cutaneous, visceral, and mucosal variants, caused by protozoan parasites of the genus that are transmitted through the bites of infected female phlebotomine sandflies. This pentavalent antimonial compound has been a cornerstone therapy since the mid-20th century, targeting intracellular amastigotes in macrophages to alleviate symptoms such as skin ulcers in cutaneous cases, organ involvement like in (also known as kala-azar), and destructive lesions in mucosal forms. The drug demonstrates efficacy against Leishmania species prevalent in both Old World (e.g., L. major, L. tropica in , , and the ) and New World (e.g., L. braziliensis, L. mexicana in the ) regions, making it suitable for diverse epidemiological contexts. It remains a first-line therapy in many resource-limited endemic areas, particularly where access to alternatives is constrained, despite reports of emerging antimonial resistance in certain foci such as , . Recent guidelines as of 2024 from PAHO and CDC recommend it where alternatives like liposomal are unavailable or contraindicated, but prefer less toxic options in other settings. In alternative contexts, sodium stibogluconate has received designation from the for the treatment of (AML), based on preclinical evidence of its potential as a inhibitor targeting leukemic cells, though clinical evidence remains limited and it is not a standard therapy. Its use is often prioritized when other agents, such as or liposomal , are unavailable, contraindicated, or ineffective due to regional resistance patterns, ensuring targeted application in high-burden settings.

Contraindications and precautions

Sodium stibogluconate is contraindicated in patients with known to antimonials or any components of the formulation, as this can lead to severe allergic reactions. It is also absolutely contraindicated in individuals with significant hepatic impairment or severe renal dysfunction, due to the risk of exacerbated toxicity from impaired drug clearance. It is contraindicated in breast-feeding, as the drug is excreted in breast milk. Use during pregnancy is contraindicated (category X per expert sources), unless the potential benefit outweighs the risk given limited safety data and potential fetal risks. Patients with pre-existing cardiac conditions, such as arrhythmias or risk factors for QT interval prolongation, warrant special precaution, as the drug can induce ECG changes including T-wave alterations and ST depression. Additionally, caution is advised in those with malnutrition or severe debilitation, where toxicity thresholds may be lower. Drug interactions that increase risk include concomitant administration with , which can heighten and ; a 14-day washout period is recommended between treatments. Concurrent use with other QT-prolonging agents, such as or certain antimalarials, should be avoided to prevent potentially fatal ventricular arrhythmias. Additive renal toxicity may occur with other nephrotoxic drugs, necessitating careful monitoring. Given its primary renal excretion, with over 80% of the dose cleared via the kidneys within the first few hours of administration, baseline assessment and periodic monitoring of renal function (e.g., serum creatinine) are essential. Patients should undergo baseline and regular ECG evaluations to detect cardiac effects, along with (e.g., transaminases) and serum amylase levels to monitor for and , respectively. Complete blood counts should also be checked periodically for hematologic abnormalities.

Adverse effects

Common side effects

Sodium stibogluconate therapy is frequently associated with gastrointestinal effects, including anorexia, , , , and , which occur in 10-20% of patients and can affect up to 50% in some cohorts depending on dose and duration. These symptoms are typically mild to moderate, dose-related, and often managed with antiemetics or dietary adjustments, resolving shortly after treatment completion. Musculoskeletal effects such as , , and general body aches are among the most prevalent, reported in 49-59% of patients, particularly during the later stages of the 20-day treatment course. These complaints are usually transient and self-limiting, subsiding post-treatment without long-term sequelae, though nonsteroidal drugs may provide symptomatic relief. General symptoms like , (or ), and fever are also common, affecting 17-67% of patients and often peaking mid-treatment due to cumulative toxicity. These are generally manageable with supportive care such as , hydration, and antipyretics, and they tend to be dose-dependent rather than indicative of severe . Local reactions at the administration site are frequent, with intramuscular injections causing pain in up to 29% of cases and intravenous use leading to irritation, flushing, or in a similar proportion. These effects are localized, mild, and typically resolve without intervention, though slower infusion rates can mitigate intravenous discomfort.

Serious side effects

Serious side effects of sodium stibogluconate are uncommon but can be life-threatening, often necessitating hospitalization, treatment discontinuation, or intensive monitoring. These primarily include cardiac arrhythmias, , and organ toxicities affecting the liver and kidneys, with fatalities reported in rare cases linked to cumulative dosing or underlying comorbidities. Cardiac toxicity manifests as dose-dependent QT interval prolongation, observed in approximately 13% of patients during therapy, with corrected QT intervals reaching up to 524 ms. This can progress to , , or sudden death, particularly in those with pre-existing cardiac conditions; electrocardiographic monitoring is essential during infusion to detect these changes early. Pancreatic toxicity involves elevations in serum and levels, occurring in up to 94-100% of treated patients in clinical studies, with developing symptomatically in 34-71% of cases, characterized by and . These enzyme rises typically peak during the second week of treatment and may resolve upon discontinuation, though therapy interruption is often required. Hepatic and renal effects include transient elevations in liver enzymes such as ALT, with mean peaks around 107 IU/L observed by day 13 of treatment, rarely progressing to clinical . Renal impairment, including and tubular , can occur, particularly with prolonged courses exceeding 20 days, leading to hyperchloremic in susceptible patients. Other serious reactions encompass , affecting about 3% of patients with platelet counts dropping below 100,000/µL without associated bleeding, and rare presenting as during infusion. Patients with cardiac disease should avoid sodium stibogluconate due to heightened risk, as noted in contraindications.

Administration and dosing

Dosage regimens

The standard dosage regimen for sodium stibogluconate in the treatment of is 20 mg of pentavalent (Sb(V)) per kg body weight daily, administered intravenously or intramuscularly, with no upper dose limit. The duration of therapy depends on the form of leishmaniasis: typically 20 days for and 28 days for visceral or mucosal leishmaniasis. In cutaneous cases from certain regions, a 21-day course may be recommended. Pediatric dosing follows the same mg/kg regimen as for adults. For patients with renal impairment, dose reduction should be considered to avoid , and the is contraindicated in cases of significant renal failure. In resistant or complicated cases, particularly , combination therapy is frequently employed; for example, sodium stibogluconate at 20 mg Sb(V)/kg/day combined with at 15 mg/kg/day intramuscularly for 17 days has been adopted as first-line treatment in .

Administration methods

Sodium stibogluconate is administered via intravenous (IV) or intramuscular (IM) routes, with the IV route preferred to minimize pain associated with injection. For cutaneous leishmaniasis with few lesions, intralesional administration may be used as an alternative, injecting 0.5–5 mL per lesion (up to 4–5 sites) and repeating every 3–7 days until healing. The IV infusion must be administered slowly, over 10–30 minutes, to reduce the risk of local thrombosis and cardiac effects. Intramuscular administration is reserved for settings where IV access is not feasible, such as remote field conditions, and involves deep injection into the gluteal muscle; if the volume exceeds 10 mL, the dose should be split between two sites to lessen discomfort and tissue damage. Prior to administration, the solution must be filtered using a 5-micron or smaller pore-size filter to remove particulates, with an in-line filter recommended for IV use. For IV infusion, the drug is diluted in 50–100 mL of 5% dextrose in (D5W) to facilitate safe delivery and prevent irritation. The preparation is stable at (below 25°C), but must be protected from light and not frozen; once a is opened, the contents should be used within one month. During administration, particularly via IV, electrocardiogram (ECG) monitoring is recommended before and during therapy to detect potential QTc prolongation or arrhythmias, with checked regularly and the infusion halted immediately if signs of , such as or , emerge. This cardiac vigilance is critical given the drug's association with serious adverse effects like .

Pharmacology

Pharmacodynamics

Sodium stibogluconate, a pentavalent antimony compound (Sb(V)), exerts its antileishmanial effects primarily through disruption of energy metabolism in Leishmania parasites. It inhibits key enzymes in glycolysis and the citric acid cycle, leading to a significant reduction in ATP and GTP levels by 56–65%, which impairs the phosphorylation of ADP and subsequently hampers the synthesis of macromolecules such as DNA, RNA, and proteins by 51–65% following exposure to 500 µg/ml Sb for 4 hours. This metabolic interference results in decreased parasite viability, with amastigotes showing 40–61% loss under similar conditions. The drug demonstrates target specificity by preferentially accumulating in the intracellular amastigote form of Leishmania, the clinically relevant stage, at concentrations that exceed those in host macrophages. Once inside the parasite, Sb(V) is likely reduced to the more toxic trivalent form (Sb(III)), which exerts a dual action on thiol redox metabolism: it inhibits trypanothione reductase (TR), a flavoprotein enzyme unique to kinetoplastids that maintains the reduced pool of trypanothione for antioxidant defense, and it induces rapid efflux of trypanothione and glutathione, depleting intracellular thiol buffering capacity. Additionally, pentavalent antimony inhibits type I DNA topoisomerase in Leishmania, preventing DNA relaxation and leading to DNA damage. This selective targeting exploits the parasite's reliance on trypanothione-based redox homeostasis, absent in mammalian cells. Resistance to sodium stibogluconate in arises from multiple mechanisms that reduce intracellular drug accumulation. Mutations in the aquaglyceroporin 1 (AQP1) , which encodes a channel facilitating Sb(III) uptake, diminish drug influx and are a proven marker of antimony resistance in clinical isolates. Additionally, overexpression of efflux pumps, such as the ATP-binding cassette transporter MRPA (also known as PGPA or ABCC3), sequesters -thiol conjugates into intracellular vesicles for extrusion, further decreasing cytosolic Sb(III) levels and contributing to treatment failure. Beyond its primary antiparasitic role, sodium stibogluconate exhibits limited activity against other , such as species, due to lower efficacy in inhibiting their distinct metabolic pathways. Investigational studies have explored its potential anticancer effects, particularly in (AML) cells, alongside its known inhibition of protein tyrosine phosphatases to promote differentiation and responses.

Pharmacokinetics

Sodium stibogluconate has poor oral bioavailability and is administered exclusively by intramuscular or intravenous routes, achieving complete bioavailability via these parenteral methods. Following intramuscular administration, absorption is rapid, with peak plasma concentrations attained within 0.5 to 2 hours and an absorption half-life of 0.36 to 0.85 hours. The drug distributes widely to tissues such as the liver, spleen, and skin, with highest accumulation observed in the liver followed by the thyroid and heart; skin penetration is complete relative to plasma exposure. The apparent volume of distribution is approximately 0.5 to 1 L/kg, consistent with extravascular distribution. Sodium stibogluconate crosses the blood-brain barrier poorly. In vivo, pentavalent (Sb(V)) from sodium stibogluconate is reduced intracellularly to trivalent (Sb(III)), the active form responsible for antileishmanial activity; no hepatic metabolism occurs. Elimination is primarily renal, with 40% to 80% of the dose excreted unchanged as Sb(V) via glomerular filtration; total body clearance ranges from 0.086 to 0.144 L/h/kg. The initial plasma half-life of Sb(V) is approximately 2 hours, while the terminal extends to 1 to 3 days due to slow release of intracellular Sb(III); daily dosing results in minimal accumulation owing to the predominant short elimination phase. In patients with renal impairment, such as glomerular filtration rates around 16 mL/min, the prolongs significantly to about 15 hours, requiring dose adjustments to prevent .

Chemistry

Chemical structure

Sodium stibogluconate is a pentavalent complex with the empirical molecular formula approximately C₁₂H₃₆Na₃O₂₆Sb₂ for the form and a of approximately 908 g/mol. The compound consists of Sb(V) ions complexed with gluconate ligands derived from , forming a mixture of rather than a single discrete . Its exact structure remains ambiguous due to this heterogeneity, with revealing oligomeric complexes in various Sb(V)-to-gluconate ratios, including 1:1 (monogluconate), 1:2 (digluconate), 2:2, and 2:3 forms. The material exhibits polymeric character, potentially involving chained Sb(V)-gluconate units linked through oxygen bridges, though direct Sb-O-Sb bonds between two atoms are not conclusively supported. Batch-to-batch variations in composition further complicate structural elucidation, with content typically ranging from 32% to 34%. In proposed structural models, each Sb(V) center adopts an octahedral , binding to the carboxylate oxygen and multiple hydroxyl groups of the gluconate , which chelates via its α-hydroxy acid functionality. A representative dimeric motif, often idealized in depictions, features two Sb(V) atoms bridged by an oxygen atom, with each coordinated to a single gluconate through the deprotonated carboxylic group and adjacent hydroxy groups, balanced by sodium counterions. This configuration underscores the compound's ionic and potentially oligomeric nature in .

Physical and chemical properties

Sodium stibogluconate appears as a to off-white, odorless . It exhibits high in , allowing concentrations suitable for parenteral administration (exceeding 300 mg/mL based on formulation requirements), while being practically insoluble in alcohol and most organic solvents. The compound remains stable at (up to 25°C) when stored as a solid, but aqueous solutions are light-sensitive and require protection from direct light to prevent degradation; it decomposes in the presence of strong acids or bases. For clinical use, it is prepared as an aqueous injection with a range of 5.0 to 5.5, typically at a concentration of 100 mg of pentavalent per mL. In terms of reactivity, sodium stibogluconate is incompatible with strong oxidizing agents and ; heating may lead to the formation of toxic oxides.

History and society

Development and approval

Antimonial compounds were first explored for the treatment of in the early 1900s, with trivalent sodium antimonial used as early as 1905. Sodium stibogluconate, a pentavalent antimonial, was first synthesized in the mid-1940s as part of efforts to develop effective treatments for . During , British researcher Leonard G. Goodwin at the Laboratories of advanced the clinical development of sodium stibogluconate, testing pentavalent compounds in Syrian hamsters to evaluate efficacy against parasites. These efforts addressed outbreaks among Allied troops, including British forces in , where field trials in the demonstrated its effectiveness in treating cutaneous and , leading to its production as Pentostam for military use. Sodium stibogluconate has never received formal approval from the and was previously available in the United States only through the Centers for Disease Control and Prevention under an protocol for compassionate use. It was added to the World Health Organization's Model List of Essential Medicines in 1977 for visceral and and has been reaffirmed on subsequent lists, including the 24th edition in 2025. Widespread resistance to sodium stibogluconate emerged in the 2000s, particularly in , , where treatment failure rates reached up to 65% in hyperendemic areas, and in parts of Brazil, where it affected Leishmania braziliensis infections. This prompted the adoption of combination therapies, such as with , to improve outcomes and combat resistance.

Availability and brand names

Sodium stibogluconate is available through restricted distribution channels, primarily via the (WHO) for use in endemic regions. In the United States, supply through the CDC was discontinued after 2020 due to manufacturing issues, with the IND protocol closed; alternatives must be sought. It is not commercially marketed in many countries due to its niche application in treatment and the discontinuation of large-scale manufacturing by GlaxoSmithKline (GSK) in 2020, stemming from challenges in sourcing raw materials. Despite this, generic versions continue to be produced and used in leishmaniasis-endemic regions, supported by international aid, though disruptions persist in remote areas. The primary brand name is Pentostam, originally produced by GSK in the , with generic versions of sodium stibogluconate widely utilized in leishmaniasis-endemic regions such as , , and parts of to ensure affordability and availability. These generics have been shown to be comparable in safety and efficacy to the branded product in clinical settings. Treatment courses are provided at low cost through WHO programs, approximately $15–30 per adult regimen for generics, though supply chain inefficiencies in remote endemic areas often exacerbate access barriers, including procurement delays and distribution limitations. The drug holds designation in the United States for and remains investigational for (AML).

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