Cyanocobalamin — essential cofactor for methionine synthase and methylmalonyl-CoA mutase. Used as a reference compound in B12 research and as a control in metabolic and neurological study designs.
Vitamin B12 (Cyanocobalamin) is a research compound available through our china peptide catalog as a finished, lyophilized vial from an established Chinese manufacturer. It belongs to the Cobalamin (vitamin B12 vitamer, synthetic stable form)
Research Areas
One-carbon metabolism, homocysteine biology, methylation research, neurological function, B12 deficiency models
Available Variants
| Name | Strength | Pack Size | Purity | Availability |
|---|---|---|---|---|
| Vitamin B12 (Cyanocobalamin) | 10 mg | 10 vials | ≥98% | In Stock |
Specification Highlights
Quality & Testing
Testing method: HPLC / LC-MS . Products are supplied against the specification shown on the applicable product page. The standard catalog purity specification is ≥98% unless otherwise stated. Product-specific specifications and quality-control information may vary by compound and batch. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control, using methods such as HPLC and LC-MS. These results are kept in the manufacturer’s internal quality-control records and are not issued as a separate certificate or document.
Research Areas
One-Carbon Metabolism and Methylation Research Methylcobalamin is the cofactor for methionine synthase — the enzyme that regenerates methionine from homocysteine using 5-methyltetrahydrofolate as the methyl donor. This reaction is the central node of one-carbon metabolism: it connects the folate cycle (methylenetetrahydrofolate reductase, MTHFR) to the methionine cycle (SAM production, SAM-dependent methylation). Research using B12-deficient cell cultures and animal models defines how B12 availability affects SAM/SAH ratios, global DNA methylation, and gene expression in metabolic and neurological research contexts. Neurological Function and Myelin Research B12 deficiency produces subacute combined degeneration of the spinal cord — a neurological syndrome reflecting the role of methylcobalamin in myelin maintenance. Research has examined the mechanistic link between B12-dependent methylation reactions and myelin basic protein gene expression, and between elevated methylmalonic acid (from adenosylcobalamin deficiency) and neuronal mitochondrial function. B12-deficient rodent models are used to study the neurostructural consequences of methylation cycle blockade. Homocysteine Biology and Cardiovascular Research Hyperhomocysteinemia — elevated plasma homocysteine — is an established marker of B12/folate deficiency and a cardiovascular risk factor in epidemiological research. Studies have examined how homocysteine affects endothelial function, platelet activation, oxidative stress (homocysteine auto-oxidizes to generate superoxide), and smooth muscle cell proliferation. B12 treatment as a homocysteine-lowering intervention in these models provides mechanistic insight into the relationship between one-carbon metabolism and vascular biology. ## Sourcing Vitamin B12 (Cyanocobalamin) From China
Vitamin B12 (Cyanocobalamin) is available through our platform as a china peptide sourced directly from an established Chinese manufacturer. Three points define how we handle it:
- Factory-direct, not trader-sourced. We confirm availability and specification with the manufacturer before the order is confirmed. There is no intermediary resale of unknown-origin vials in this catalog.
- Specification before shipment. The purity and concentration specification shown on this page is the manufacturer’s batch specification. Product-specific quality-control information travels with the order.
- Research-use discipline. Like every listing in our catalog, Vitamin B12 (Cyanocobalamin) is supplied for laboratory research use only, under strict research-use terms.
For buyers comparing chinese peptides suppliers, the practical test is whether the seller can name the manufacturer and show the batch documentation. We work the other way around: the manufacturer and the documentation are the offer. Browse the full catalog or see how sourcing works.
Available Variants
| Name | Strength | Pack Size | Purity | Availability |
|---|---|---|---|---|
| Vitamin B12 (Cyanocobalamin) | 10 mg | 10 vials | ≥98% | In Stock |
Specification Highlights
Quality & Testing
Testing method: HPLC / LC-MS . Products are supplied against the specification shown on the applicable product page. The standard catalog purity specification is ≥98% unless otherwise stated. Product-specific specifications and quality-control information may vary by compound and batch. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control, using methods such as HPLC and LC-MS. These results are kept in the manufacturer’s internal quality-control records and are not issued as a separate certificate or document.
Research Areas
One-Carbon Metabolism and Methylation Research Methylcobalamin is the cofactor for methionine synthase — the enzyme that regenerates methionine from homocysteine using 5-methyltetrahydrofolate as the methyl donor. This reaction is the central node of one-carbon metabolism: it connects the folate cycle (methylenetetrahydrofolate reductase, MTHFR) to the methionine cycle (SAM production, SAM-dependent methylation). Research using B12-deficient cell cultures and animal models defines how B12 availability affects SAM/SAH ratios, global DNA methylation, and gene expression in metabolic and neurological research contexts. Neurological Function and Myelin Research B12 deficiency produces subacute combined degeneration of the spinal cord — a neurological syndrome reflecting the role of methylcobalamin in myelin maintenance. Research has examined the mechanistic link between B12-dependent methylation reactions and myelin basic protein gene expression, and between elevated methylmalonic acid (from adenosylcobalamin deficiency) and neuronal mitochondrial function. B12-deficient rodent models are used to study the neurostructural consequences of methylation cycle blockade. Homocysteine Biology and Cardiovascular Research Hyperhomocysteinemia — elevated plasma homocysteine — is an established marker of B12/folate deficiency and a cardiovascular risk factor in epidemiological research. Studies have examined how homocysteine affects endothelial function, platelet activation, oxidative stress (homocysteine auto-oxidizes to generate superoxide), and smooth muscle cell proliferation. B12 treatment as a homocysteine-lowering intervention in these models provides mechanistic insight into the relationship between one-carbon metabolism and vascular biology.
Compound Profile
Cyanocobalamin is the synthetic, most stable form of vitamin B12 — a water-soluble organometallic coenzyme with a cobalt center coordinated in a corrin ring. Cyanocobalamin is distinguished from other B12 vitamers (methylcobalamin, adenosylcobalamin, hydroxocobalamin) by the cyano ligand bound to cobalt; in the body, cyanocobalamin is converted to the active coenzyme forms methylcobalamin and 5-deoxyadenosylcobalamin. These active forms serve as cofactors for two critical enzymatic reactions: methionine synthase (methylcobalamin — remethylation of homocysteine to methionine, essential for SAM production and one-carbon metabolism) and methylmalonyl-CoA mutase (adenosylcobalamin — isomerization of methylmalonyl-CoA to succinyl-CoA, essential for amino acid and odd-chain fatty acid catabolism). Research interest in cyanocobalamin and vitamin B12 spans one-carbon metabolism, neurological function, and methylation research. B12 deficiency produces two distinct biochemical defects: elevated homocysteine (methylation pathway blockade, measurable as hyperhomocysteinemia) and elevated methylmalonic acid (MMA — odd-chain fatty acid catabolism blockade, measurable by urine/plasma MMA). These biochemical markers are used in research to assess B12 adequacy and to study the downstream effects of B12 deficiency on DNA methylation, neurological integrity, and cardiovascular risk markers. Cyanocobalamin injection preparations deliver B12 systemically without dependence on intrinsic factor-mediated intestinal absorption. Peptides of China supplies Cyanocobalamin (Vitamin B12) as a lyophilized powder or injectable formulation at verified concentration. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control. All products are for laboratory research use only and are not for human consumption.
Profile
Research Areas
One-carbon metabolism, homocysteine biology, methylation research, neurological function, B12 deficiency models
Available Variants
| Name | Strength | Pack Size | Purity | Availability |
|---|---|---|---|---|
| Vitamin B12 (Cyanocobalamin) | 10 mg | 10 vials | ≥98% | In Stock |
Specification Highlights
Quality & Testing
Testing method: HPLC / LC-MS . Products are supplied against the specification shown on the applicable product page. The standard catalog purity specification is ≥98% unless otherwise stated. Product-specific specifications and quality-control information may vary by compound and batch. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control, using methods such as HPLC and LC-MS. These results are kept in the manufacturer’s internal quality-control records and are not issued as a separate certificate or document.
Research Areas
One-Carbon Metabolism and Methylation Research Methylcobalamin is the cofactor for methionine synthase — the enzyme that regenerates methionine from homocysteine using 5-methyltetrahydrofolate as the methyl donor. This reaction is the central node of one-carbon metabolism: it connects the folate cycle (methylenetetrahydrofolate reductase, MTHFR) to the methionine cycle (SAM production, SAM-dependent methylation). Research using B12-deficient cell cultures and animal models defines how B12 availability affects SAM/SAH ratios, global DNA methylation, and gene expression in metabolic and neurological research contexts. Neurological Function and Myelin Research B12 deficiency produces subacute combined degeneration of the spinal cord — a neurological syndrome reflecting the role of methylcobalamin in myelin maintenance. Research has examined the mechanistic link between B12-dependent methylation reactions and myelin basic protein gene expression, and between elevated methylmalonic acid (from adenosylcobalamin deficiency) and neuronal mitochondrial function. B12-deficient rodent models are used to study the neurostructural consequences of methylation cycle blockade. Homocysteine Biology and Cardiovascular Research Hyperhomocysteinemia — elevated plasma homocysteine — is an established marker of B12/folate deficiency and a cardiovascular risk factor in epidemiological research. Studies have examined how homocysteine affects endothelial function, platelet activation, oxidative stress (homocysteine auto-oxidizes to generate superoxide), and smooth muscle cell proliferation. B12 treatment as a homocysteine-lowering intervention in these models provides mechanistic insight into the relationship between one-carbon metabolism and vascular biology.