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B12

Cyanocobalamin or methylcobalamin. Cofactor in methylation and hematopoiesis pathways.

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At a glance

B12 by the numbers

The key figures from our lexicon. Drag the point along the curve to see how much is left after one dose, by calculation.

Full lexicon entry

How long does it stay in the body?

Share left after one dose, calculated with a half-life of ~6 days

Half-life ~6 days
After 12 days: 25 %
Day 6 · 50 %Day 12 · 25 %Day 18 · 12.5 %Day 30 · 3.1 %

Simplified model without an absorption phase, half-life from the TPD lexicon.

Class
Water-soluble vitamin

Cobalamin

Half-life
~6 days

B12 binds to transcobalamin

Use
Energy metabolism

neurological function

Sizes
2 sizes

10ml/1mg/ml, 10ml/10mg/ml

For research and educational purposes only. Values from the TPD lexicon, sources linked there.

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Knowledge

Everything about B12

Description

B12 (cobalamin) is a water-soluble vitamin and cofactor in two central enzymatic reactions: methionine synthase (methylation pool regulation) and methylmalonyl-CoA mutase (fatty acid metabolism). Structurally, the molecule possesses a corrin ring with a central cobalt atom, making it one of the largest vitamin molecules. In research context, B12 is used as a pure metabolic cofactor, not as a peptide.

The two most common B12 forms in research settings are cyanocobalamin (synthetic form, well storable) and methylcobalamin (already methylated active form). The choice between the two depends on the research design. Methylcobalamin bypasses initial activation steps and is more directly available in the methylation pool.

The research mechanism lies in the methylation axis: B12 enables the conversion of homocysteine to methionine and thus the regeneration of the SAM pool (S-adenosylmethionine), which is the central methyl donor for hundreds of cellular reactions. In research setups investigating methylation status, homocysteine levels or one-carbon metabolism, B12 is an established tool.

In preclinical models, B12 deficiency has documented effects on hematopoiesis, nerve myelination and cognitive endpoints. B12 supplementation addresses these pathways accordingly.

B12 is available in 10ml vials as 10-vial packs, with either 1 mg/ml or 10 mg/ml.

This information is for research and educational purposes only. No medical recommendations.

Risks & Safety

B12 is considered remarkably well tolerated per study reports. As a water-soluble vitamin, an excess is largely excreted renally according to the literature. No pronounced toxicity profile is described.

Observed in studies and user reports:

  • Injection site: mild redness, pressure or transient irritation at the injection site is the most common observation.
  • Transient reactions: a sensation of warmth or mild tingling shortly after application is occasionally reported.
  • Sensitivity reactions: in rare cases the literature describes reactions to the active substance or the vehicle.
  • Long-term data: B12 as a cofactor is mechanistically well characterized, yet specific data on very long-term injectable use in research settings remain limited.

This classification does not replace medical advice. Risk and responsibility for any actual use lie entirely with the buyer.

Studies

  • Vitamin B12 deficiency - Nature Reviews Disease Primers 2017: Review: B12 plays a central role in DNA synthesis, methylation and mitochondrial metabolism. Biomarkers of B12 status include total B12, transcobalamin-bound B12, homocysteine and methylmalonic acid.
  • The many faces of vitamin B12: catalysis by cobalamin-dependent enzymes - Annual Review of Biochemistry 2003: Review of the enzymology: cobalamin serves as a cofactor for adenosylcobalamin-dependent isomerases, methylcobalamin-dependent methyltransferases and dehalogenases, each exploiting a different cleavage of the cobalt-carbon bond.
  • Vitamin B12, folate, and the methionine remethylation cycle - biochemistry, pathways, and regulation - Journal of Inherited Metabolic Disease 2019: Review of cobalamin metabolism: B12 is the cofactor of methionine synthase and of mitochondrial methylmalonyl-CoA mutase. Methionine synthase remethylates homocysteine to methionine and thereby supplies S-adenosylmethionine as the main methyl donor.
  • Oral vitamin B12 versus intramuscular vitamin B12 for vitamin B12 deficiency - Cochrane Database of Systematic Reviews 2018: Cochrane review of three randomized trials with 153 participants comparing oral and intramuscular administration: no clinically relevant difference in serum levels in two trials and higher levels with high-dose oral B12 in the third, with low-quality evidence.

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FAQ

Frequently asked

Sources for every answer: lexicon entry

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What does the body need B12 for?

B12 is a helper for two enzymes. Methylmalonyl-CoA mutase breaks down certain amino acids in the mitochondria. Methionine synthase converts homocysteine into methionine, from which the cell's most important methyl donor is made. This affects DNA synthesis, blood formation and nerves.

Is an injection better than a tablet?

Not necessarily. In a trial with 33 evaluable people with deficiency the B12 level after 4 months was 1,005 pg/ml with a high daily tablet amount and 325 pg/ml with injections into the muscle. Blood count and nerves improved equally fast. A Cochrane review of 3 trials with 153 participants sees both routes as similar but rates the evidence as weak.

Who is more often low in B12?

According to a review mainly older adults, plus people who eat few animal foods and anyone with impaired absorption. In a trial over more than 4 years metformin lowered B12 by 19 percent versus placebo, the risk of deficiency rose by 7.2 percentage points.

What does B12 have to do with homocysteine?

Without B12 the breakdown of homocysteine stalls and the blood level rises. In a meta-analysis of 1,114 people folic acid lowered homocysteine by 25 percent, extra B12 by a further 7 percent. Whether lower homocysteine also protects the heart and vessels is not answered by this work.

Does B12 give more energy without a deficiency?

The sources here give no evidence for that. The studies concern people with deficiency or specific diseases. In early ALS methylcobalamin, a different B12 form in a very high amount, slowed the loss of function over 16 weeks by 1.97 points versus placebo. That cannot be transferred to healthy people.

Which side effects are known?

Hardly any in the comparison trials: one trial saw no treatment-related side effects, in another 2 of 30 people on tablets stopped because of side effects. The quality of these data is very low. In the ALS trial side effects occurred about as often on methylcobalamin as on placebo.

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