Target intelligence / Profile preview

Vitamin B12 pathway

Molecular classification
Other
01

Overview

The "Vitamin B12 pathway" encompasses the coordinated actions of proteins and enzymes that enable the absorption, transport, intracellular utilization, and recycling of vitamin B12 (cobalamin). Dietary B12 is released from proteins in food by gastric acid and proteases, binds first to haptocorrin (also called R-binder), and then to intrinsic factor (produced by parietal cells). The vitamin B12–intrinsic factor complex is absorbed in the terminal ileum via receptor-mediated endocytosis involving cubam (cubilin/amnionless complex). After absorption, B12 is transferred to transcobalamin II and distributed to tissues, where it serves as a cofactor for methionine synthase (required for methylation reactions and DNA synthesis) and methylmalonyl-CoA mutase (required for odd-chain fatty acid and amino acid metabolism). Deficiencies or inborn errors affecting any step may cause megaloblastic anemia, neuropathy, and other disease states. Because this is a collection of processes involving multiple molecular targets rather than a single protein or defined target, it is not considered a canonical molecular target for drug discovery but rather a biological pathway.

Other names
Vitamin B12 metabolismCobalamin pathwayCobalamin absorption pathwayVitamin B12 transport
02

Mechanism of action

Supplementation supplies the cofactor for essential enzymes: Methionine synthase (methylates homocysteine to methionine, using methylcobalamin) Methylmalonyl-CoA mutase (converts methylmalonyl-CoA to succinyl-CoA, using adenosylcobalamin)

03

Biological functions

Vitamin absorptionCofactor metabolismMethylation reactionsDNA synthesisFatty acid metabolismAmino acid metabolismEnergy production
04

Disease associations

Megaloblastic anemiaHomocystinuriaNeuropathy/neurodegenerationCardiovascular diseaseOther (various inborn errors of metabolism and malabsorption syndromes)
05

Safety considerations

Deficiency is common in vegans, the elderly, and patients with absorption disorders; can cause irreversible neurological damage if untreatedOver-supplementation is generally well-tolerated but may rarely cause acneiform eruptions or hypersensitivity.Correcting B12 levels may mask hematological signs of folate deficiency but not prevent neurological damage from it.
06

Interacting drugs

Cobalamin (various formulations: cyanocobalamin, methylcobalamin, hydroxocobalamin, adenosylcobalamin; these are vitamin B12 supplements)

1 more in the full profile.

07

Biomarkers

Serum vitamin B12Methylmalonic acid (elevated in deficiency)HomocysteineHolotranscobalamin

Beyond the preview

Go deeper on Vitamin B12 pathway.

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Vitamin B12 pathway.

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call