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- Chromous sulfate
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Chromous sulfate | CAS No: 13825-86-0 | GMP-certified suppliers
A medication that supplements chromium in total parenteral nutrition to maintain serum levels, prevent deficiency symptoms, and support glucose metabolism in patients requiring intravenous nutrition.
Therapeutic categories
Drugs that are Mainly Renally Excreted
Generic name
Chromous sulfate
Molecule type
small molecule
CAS number
13825-86-0
DrugBank ID
DB14530
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
- Chromous sulfate is formulated as an injectable inorganic salt for use in intravenous solutions
- It is primarily used as a supplement in total parenteral nutrition (TPN) to maintain chromium serum levels and prevent deficiency
- This product is approved for use by the U
Clinical Overview
Chromous sulfate (CAS Number 13825-86-0) is an inorganic compound classified as a transition metal sulfate. It contains trivalent chromium, an essential trace element involved in glucose and lipid metabolism. Chromous sulfate is indicated for use as a supplement in intravenous solutions administered for total parenteral nutrition (TPN). Its purpose is to maintain chromium serum levels and prevent depletion of endogenous chromium stores, thereby averting deficiency-related symptoms.
Pharmacodynamically, trivalent chromium acts as a component of the glucose tolerance factor, enhancing insulin-mediated biochemical reactions. It facilitates normal glucose metabolism and supports peripheral nerve function. Chromium increases insulin binding to target cells by upregulating insulin receptor density and activating insulin receptor kinase, which leads to improved insulin sensitivity. Clinical observations have shown that intravenous administration of chromium in deficient patients normalizes the glucose tolerance curve, reversing diabetic-like disturbances caused by chromium deficiency.
The mechanism of action of chromous sulfate involves potentiation of insulin signaling pathways. Chromium enhances insulin-stimulated signal transduction by affecting downstream effector molecules within the insulin receptor (IR)-mediated cascade. Activation of the IR triggers autophosphorylation of its β-subunit and initiates a cascade involving protein kinases such as phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). This cascade ultimately promotes translocation of glucose transporter-4 (GLUT-4) vesicles to the plasma membrane, increasing glucose uptake into muscle cells. Chromium also exerts effects independent of traditional insulin signaling proteins under insulin-resistant conditions by facilitating cholesterol efflux and membrane fluidity, which promotes GLUT-4 translocation. Additional mechanisms include inhibition of protein tyrosine phosphatase-1B (PTP-1B), alleviation of endoplasmic reticulum stress, and transient activation of AMP-activated protein kinase (AMPK), all contributing to enhanced glucose metabolism.
Chromous sulfate is primarily eliminated via renal excretion, aligning it with drugs mainly cleared through the kidneys. Safety considerations focus on maintaining therapeutic serum chromium levels to avoid both deficiency and potential toxicity; monitoring chromium status is advisable in patients receiving prolonged or high-dose TPN supplementation.
This compound is approved for medical use, though it is not associated with specific proprietary brand names. In sourcing chromous sulfate active pharmaceutical ingredient (API), quality assurance must address stringent control of elemental chromium valence state and sulfate purity, as well as adherence to established pharmacopeial standards to ensure consistency and safety in parenteral formulations.
Pharmacodynamically, trivalent chromium acts as a component of the glucose tolerance factor, enhancing insulin-mediated biochemical reactions. It facilitates normal glucose metabolism and supports peripheral nerve function. Chromium increases insulin binding to target cells by upregulating insulin receptor density and activating insulin receptor kinase, which leads to improved insulin sensitivity. Clinical observations have shown that intravenous administration of chromium in deficient patients normalizes the glucose tolerance curve, reversing diabetic-like disturbances caused by chromium deficiency.
The mechanism of action of chromous sulfate involves potentiation of insulin signaling pathways. Chromium enhances insulin-stimulated signal transduction by affecting downstream effector molecules within the insulin receptor (IR)-mediated cascade. Activation of the IR triggers autophosphorylation of its β-subunit and initiates a cascade involving protein kinases such as phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). This cascade ultimately promotes translocation of glucose transporter-4 (GLUT-4) vesicles to the plasma membrane, increasing glucose uptake into muscle cells. Chromium also exerts effects independent of traditional insulin signaling proteins under insulin-resistant conditions by facilitating cholesterol efflux and membrane fluidity, which promotes GLUT-4 translocation. Additional mechanisms include inhibition of protein tyrosine phosphatase-1B (PTP-1B), alleviation of endoplasmic reticulum stress, and transient activation of AMP-activated protein kinase (AMPK), all contributing to enhanced glucose metabolism.
Chromous sulfate is primarily eliminated via renal excretion, aligning it with drugs mainly cleared through the kidneys. Safety considerations focus on maintaining therapeutic serum chromium levels to avoid both deficiency and potential toxicity; monitoring chromium status is advisable in patients receiving prolonged or high-dose TPN supplementation.
This compound is approved for medical use, though it is not associated with specific proprietary brand names. In sourcing chromous sulfate active pharmaceutical ingredient (API), quality assurance must address stringent control of elemental chromium valence state and sulfate purity, as well as adherence to established pharmacopeial standards to ensure consistency and safety in parenteral formulations.
Identification & chemistry
| Generic name | Chromous sulfate |
|---|---|
| Molecule type | Small molecule |
| CAS | 13825-86-0 |
| UNII | TR64E2WM7Z |
| DrugBank ID | DB14530 |
Pharmacology
| Summary | Chromium acts as an essential cofactor modulating insulin signaling pathways by enhancing insulin receptor β kinase activity and downstream effectors such as PI3K and Akt, thereby facilitating GLUT-4 translocation and glucose uptake. It also modulates membrane cholesterol content and attenuates negative regulators like PTP-1B and ER stress-associated pathways, contributing to improved insulin sensitivity under insulin-resistant conditions. Chromium is involved in maintaining normal glucose metabolism and peripheral nerve function, primarily targeting cytochrome b5. |
|---|---|
| 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
- Chromous sulfate is a small molecule inorganic compound suitable for oral or injectable formulations due to its high water solubility.
- Its negative LogP value indicates hydrophilic properties, favoring aqueous formulations.
- Handling requires consideration of transition metal reactivity and potential stability issues under oxidative conditions.
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:
- Hexavalent chromium compounds are classified as human carcinogens via inhalation and pose mutagenic risks based on in vitro and occupational studies
- Acute oral toxicity varies significantly between chromium species
- Cr (VI) exhibits substantially lower LD50 values compared to Cr (III) forms
Chromous sulfate 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.
