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- Chromium gluconate
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Chromium gluconate | CAS No: 33661-40-4 | GMP-certified suppliers
A medication that supports total parenteral nutrition by maintaining chromium serum levels to prevent deficiency and promote metabolic balance in patients requiring intravenous supplementation.
Therapeutic categories
Drugs that are Mainly Renally Excreted
Generic name
Chromium gluconate
Molecule type
small molecule
CAS number
33661-40-4
DrugBank ID
DB14528
Approval status
Approved drug
Primary indications
- Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms
Product Snapshot
- Chromium gluconate is supplied as an injectable mineral solution for intravenous use
- Its primary application is as a supplement in total parenteral nutrition formulations to maintain chromium serum levels and prevent deficiency
- This ingredient is approved for use by regulatory agencies, including the FDA
Clinical Overview
Chromium gluconate (CAS number 33661-40-4) is an inorganic salt of trivalent chromium conjugated with gluconic acid, classified within the sugar acids and derivatives chemical family. It is medically indicated as a supplement in total parenteral nutrition (TPN) protocols to maintain adequate serum chromium levels, preventing chromium depletion and associated deficiency symptoms.
Pharmacodynamically, chromium plays a critical role as a component of the glucose tolerance factor, facilitating insulin-mediated metabolic processes. It enhances insulin activity by increasing insulin receptor density on target cells, promoting insulin binding, and activating the insulin receptor’s tyrosine kinase. These effects improve cellular insulin sensitivity and help normalize glucose metabolism disrupted during chromium deficiency. Intravenous administration of chromium gluconate during chromium-deficient states has been shown to restore impaired glucose tolerance.
At the molecular level, chromium potentiates insulin signaling by influencing downstream effectors in the insulin receptor (IR) pathway. This includes activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt), which promote translocation of glucose transporter-4 (GLUT4) vesicles to the plasma membrane, increasing glucose uptake by muscle cells. Chromium additionally facilitates GLUT4 translocation independent of classical insulin signaling components by modulating membrane cholesterol and sterol regulatory element-binding proteins, promoting glucose entry under insulin-resistant conditions. It also downregulates negative insulin signaling regulators such as protein tyrosine phosphatase-1B (PTP-1B) and mitigates endoplasmic reticulum stress, which can impair insulin signaling cascades. Activation of AMP-activated protein kinase (AMPK) by chromium contributes further to glucose uptake enhancement.
Chromium gluconate is primarily eliminated via renal excretion. Safety profiles require monitoring for potential toxicity, especially in patients with compromised kidney function, as chromium accumulation may occur. Adverse effects are uncommon at physiologic supplementation levels but warrant vigilance given chromium's narrow therapeutic window.
Chromium gluconate is approved for use in clinical TPN formulations; its inclusion ensures maintenance of essential trace element balance during extended parenteral nutrition. Notable pharmaceutical preparations and clinical protocols incorporate chromium gluconate as a standard micronutrient supplement.
For API sourcing, pharmaceutical-grade chromium gluconate should comply with recognized pharmacopeial standards, exhibiting consistent purity, absence of heavy metal contaminants, and reliable bioavailability profiles. Suppliers must provide certificates of analysis confirming chromium content and impurity limits aligned with regulatory requirements to ensure safe incorporation into sterile TPN solutions.
Pharmacodynamically, chromium plays a critical role as a component of the glucose tolerance factor, facilitating insulin-mediated metabolic processes. It enhances insulin activity by increasing insulin receptor density on target cells, promoting insulin binding, and activating the insulin receptor’s tyrosine kinase. These effects improve cellular insulin sensitivity and help normalize glucose metabolism disrupted during chromium deficiency. Intravenous administration of chromium gluconate during chromium-deficient states has been shown to restore impaired glucose tolerance.
At the molecular level, chromium potentiates insulin signaling by influencing downstream effectors in the insulin receptor (IR) pathway. This includes activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt), which promote translocation of glucose transporter-4 (GLUT4) vesicles to the plasma membrane, increasing glucose uptake by muscle cells. Chromium additionally facilitates GLUT4 translocation independent of classical insulin signaling components by modulating membrane cholesterol and sterol regulatory element-binding proteins, promoting glucose entry under insulin-resistant conditions. It also downregulates negative insulin signaling regulators such as protein tyrosine phosphatase-1B (PTP-1B) and mitigates endoplasmic reticulum stress, which can impair insulin signaling cascades. Activation of AMP-activated protein kinase (AMPK) by chromium contributes further to glucose uptake enhancement.
Chromium gluconate is primarily eliminated via renal excretion. Safety profiles require monitoring for potential toxicity, especially in patients with compromised kidney function, as chromium accumulation may occur. Adverse effects are uncommon at physiologic supplementation levels but warrant vigilance given chromium's narrow therapeutic window.
Chromium gluconate is approved for use in clinical TPN formulations; its inclusion ensures maintenance of essential trace element balance during extended parenteral nutrition. Notable pharmaceutical preparations and clinical protocols incorporate chromium gluconate as a standard micronutrient supplement.
For API sourcing, pharmaceutical-grade chromium gluconate should comply with recognized pharmacopeial standards, exhibiting consistent purity, absence of heavy metal contaminants, and reliable bioavailability profiles. Suppliers must provide certificates of analysis confirming chromium content and impurity limits aligned with regulatory requirements to ensure safe incorporation into sterile TPN solutions.
Identification & chemistry
| Generic name | Chromium gluconate |
|---|---|
| Molecule type | Small molecule |
| CAS | 33661-40-4 |
| UNII | V236ZVR3RL |
| DrugBank ID | DB14528 |
Pharmacology
| Summary | Chromium functions as an essential nutrient that modulates glucose and lipid metabolism by enhancing insulin receptor kinase activity and downstream signaling pathways, including PI3K/Akt-mediated GLUT4 translocation. It also promotes glucose uptake via insulin-independent mechanisms by modulating membrane cholesterol and reducing ER stress-related inhibition of insulin signaling. Chromium’s pharmacodynamics involve increasing insulin receptor density and sensitivity, supporting maintenance of normal glucose homeostasis. |
|---|---|
| Mechanism of action | Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules . Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake . Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. Under insulin-resistant conditions, chromium also promotes GLUT-4 transporter translocation that is independent of activity of IR, IRS-1, PI3-kinase, or Akt; chromium mediates cholesterol efflux from the membranes via increasing fluidity of the membrane by decreasing the membrane cholesterol and upregulation of sterol regulatory element-binding protein . As a result, intracellular GLUT-4 transporters are stimulated to translocate from intracellular to the plasma membrane, leading to enhanced glucose uptake in muscle cells . Chromium attenuates the activity of PTP-1B _in vitro,_ which is a negative regulator of insulin signaling. It also alleviates ER stress that is observed to be elevated the suppression of insulin signaling. ER stress is thought to activate c-Jun N-terminal kinase (JNK), which subsequently induces serine phosphorylation of IRS and aberration of insulin signalling . Transient upregulation of AMPK by chromium also leads to increased glucose uptake . |
| Pharmacodynamics | Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity . In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Cytochrome b5 | Humans |
ADME / PK
| Absorption | Chromium compounds are both absorbed by the lung and the gastrointestinal tract. Oral absorption of chromium compounds in humans can range between 0.5% and 10%, with the hexavalent (VI) chromium more easily absorbed than the trivalent (III) form . Absorption of chromium from the intestinal tract is low, ranging from less than 0.4% to 2.5% of the amount consumed . Vitamin C and the vitamin B niacin is reported to enhance chromium absorption . Most hexavalent Cr (VI) undergoes partial intragastric reduction to Cr (III) upon absorption, which is an action mainly mediated by sulfhydryl groups of amino acids . Cr (VI) readily penetrates cell membranes and chromium can be found in both erythrocytes and plasma after gastrointestinal absorption of Cr (IV). In comparison, the presence of chromium is limited to the plasma as Cr (III) displays poor cell membrane penetration . Once transported through the cell membrane, Cr (VI) is rapidly reduced to Cr (III), which subsequently binds to macromolecules or conjugate with proteins. Cr (III) may be bound to transferrin or other plasma proteins, or as complexes, such as glucose tolerance factor (GTF). |
|---|---|
| Half-life | The elimination half-life of hexavalent chromium is 15 to 41 hours . |
| Protein binding | In the blood, 95% of chromium (III) is bound to large molecular mass proteins, such as transferrin, while a small proportion associates with low molecular mass oligopeptides . Serum chromium is bound to transferrin in the beta globulin fraction. |
| Metabolism | The metabolism of Cr (VI) involves reduction by small molecules and enzyme systems to generate Cr (III) and reactive intermediates. During this process, free radicals can be generated, which is thought to induce damage of cellular components and cause toxicity of chromium . The metabolites bind to cellular constituents . |
| Route of elimination | Absorbed chromium is excreted mainly in the urine, accounting for 80% of total excretion of chromium; small amounts are lost in hair, perspiration and bile . Chromium is excreted primarily in the urine by glomerular filtration or bound to a low molecular-weight organic transporter . |
| Volume of distribution | Absorbed chromium is distributed to all tissues of the body and its distribution in the body depends on the species, age, and chemical form . Circulating Cr (III) following oral or parenteral administration of different compounds can be taken up by tissues and accumulates in the liver, kidney, spleen, soft tissue, and bone . |
| Clearance | Excretion of chromium is via the kidneys ranges from 3 to 50 μg/day. The 24-hour urinary excretion rates for normal human subjects are reported to be 0.22 μg/day . |
Formulation & handling
- Chromium gluconate is a small molecule with high water solubility, suitable for oral formulations.
- Its low LogP value indicates limited lipid solubility, affecting absorption and bioavailability considerations.
- Stable under typical handling conditions without special storage requirements related to sensitivity or degradation.
Regulatory status
Safety
| Toxicity | Oral LD50 for Cr (VI) is 135 - 175 mg/kg in mouse and 46 - 113 mg/kg in rat . Oral LD50 for Cr (III) in rat is >2000 mg/kg . LD50 of chromium (III) oxide in rats is reported to be > 5g/kg . Other LD50 values reported for rats include: 3.5 g/kg (CI 3.19-3.79 g/kg) for chromium sulphate; 11.3 g/kg for chromium (III) acetate; 3.3 g/kg for chromium nitrate; and 1.5 g/kg for chromium nitrate nonahydrate . Acute overdose of chromium is rare and seriously detrimental effects of hexavalent chromium are primarily the result of chronic low-level exposure . In case of overdose with minimal toxicity following acute ingestion, treatment should be symptomatic and supportive . There is no known antidote for chromium toxicity. Hexavalent chromium is a Class A carcinogen by the inhalation route of exposure and Class D by the oral route . The oral lethal dose in humans has been estimated to be 1-3 g of Cr (VI); oral toxicity most likely involves gastrointestinal bleeding rather than systemic toxicity . Chronic exposure may cause damage to the following organs: kidneys, lungs, liver, upper respiratory tract [MSDS]. Soluble chromium VI compounds are human carcinogens. Hexavalent chromium compounds were mutagenic in bacteria assays and caused chromosome aberrations in mammalian cells. There have been associations of increased frequencies of chromosome aberrations in lymphocytes from chromate production workers . In human cells _in vitro_, Cr (VI) caused chromosomal aberrations, sister chromatid exchanges and oxidative DNA damage . |
|---|
High Level Warnings:
- 1
- Hexavalent chromium compounds exhibit significant toxicity with oral LD50 values ranging from 46 to 175 mg/kg in rodent models
- Chronic low-level exposure is primarily associated with detrimental health effects
Chromium gluconate is a type of Antimetabolites
Antimetabolites are a prominent category of pharmaceutical active pharmaceutical ingredients (APIs) utilized in the treatment of various diseases, particularly cancer. These compounds are structurally similar to naturally occurring metabolites essential for cellular processes such as DNA and RNA synthesis. By mimicking these metabolites, antimetabolites interfere with the normal functioning of cellular pathways, leading to inhibition of cancer cell growth and proliferation.
One of the widely used antimetabolites is methotrexate, a folic acid antagonist that inhibits the enzyme dihydrofolate reductase, disrupting the production of DNA and RNA. This disruption impedes the growth of rapidly dividing cancer cells. Another common antimetabolite is 5-fluorouracil (5-FU), which inhibits the enzyme thymidylate synthase, thereby interfering with DNA synthesis and inhibiting cancer cell proliferation.
Antimetabolites can be classified into several subcategories based on their mechanism of action and chemical structure. These include purine and pyrimidine analogs, folic acid antagonists, and pyrimidine synthesis inhibitors. Examples of antimetabolites in these subcategories include azathioprine, cytarabine, and gemcitabine.
Despite their effectiveness, antimetabolites can exhibit certain side effects due to their interference with normal cellular processes. These side effects may include gastrointestinal disturbances, myelosuppression (reduced production of blood cells), and hepatotoxicity.
In conclusion, antimetabolites are a vital category of pharmaceutical APIs used in the treatment of various diseases, especially cancer. By mimicking natural metabolites and disrupting crucial cellular processes, these compounds effectively inhibit cancer cell growth and proliferation. However, their usage should be carefully monitored due to potential side effects.
