Ergocalciferol Uses, Dosage, Side Effects, Food Interaction and all others data.

Ergocalciferol is an inactivated vitamin D analog. It is synthesized by some plants in the presence of UVB light. The production of ergocalciferol was prompted by the identification of dietary deficiency, more specifically vitamin D, as the main causative factor for the development of rickets. Ergocalciferol was isolated for the first time from yeast in 1931 and its structure was elucidated in 1932.

Ergocalciferol is considered the first vitamin D analog and is differentiated from cholecalciferol by the presence of a double bond between C22 and C23 and the presence of a methyl group at C24. These modifications reduce the affinity of ergocalciferol for the vitamin D binding protein resulting in faster clearance, limits its activation, and alters its catabolism.

The first approved product containing ergocalciferol under the FDA records was developed by US Pharm Holdings and was FDA approved in 1941.

Trade Name Ergocalciferol
Availability Rx and/or OTC
Generic Ergocalciferol
Ergocalciferol Other Names Activated ergosterol, Ercalciol, Ergocalciferol, Ergocalciférol, Ergocalciferolum, Oleovitamin D2, Viosterol, Vitamin D2, Vitamina D2
Related Drugs cholecalciferol, calcitriol, ferrous sulfate, folic acid, Vitamin D3, calcium carbonate, thiamine, Zinc, Caltrate, selenium
Weight 2000intlunits, 50, 000intlunits, 8000intlunits/ml
Type Oral capsule, oral solution
Formula C28H44O
Weight Average: 396.6484
Monoisotopic: 396.33921603
Protein binding

Ergocalciferol is not found significantly distributed circulating in plasma. It is known to be found in its bound form to the vitamin D plasma protein. The parent compound of ergocalciferol does not bind directly to plasma proteins, however, 70-90% of its metabolites such as cholecalciferol and calcitriol are found in the bound form.

Groups Approved, Nutraceutical
Therapeutic Class
Available Country United States
Last Updated: September 19, 2023 at 7:00 am


Ergocalciferol is a vitamin found in many supplement products.

Ergocalciferol is indicated for the treatment of hypoparathyroidism, refractory rickets, and familial hypophosphatemia.

Hypoparathyroidism is the result of inadequate parathyroid hormone production that occurs due to the presence of damage or removal of the parathyroid glands. This condition produces decreased calcium and increased phosphorus levels.

Rickets is a condition produced due to a deficiency in vitamin D, calcium or phosphorus. However, this condition can also be related to renal diseases. It is characterized to present weak or soft bones.

Familial hypophosphatemia is characterized by the impaired transport of phosphate and an altered vitamin D metabolism in the kidneys. The presence of this condition can derive in the presence of osteomalacia, bone softening and rickets.

Ergocalciferol is also used to associated treatment for these conditions: Deficiency, Vitamin A, Deficiency, Vitamin D, Hypoparathyroidism, Hypophosphatemia, Familial, Vitamin D Resistant Rickets, Dietary supplementation

How Ergocalciferol works

For its activity, ergocalciferol is required to be transformed to its major active circulating hydroxylated metabolite and transported to the target organs in order to bind to its target, the vitamin D receptor.

The activation of the vitamin D receptor is part of the vitamin D endocrine system and it is described by the production of a change in the transcription rates of the vitamin D receptor target genes. The target genes in the DNA affected by the presence of ergocalciferol are called vitamin D response elements which are dependent on co-modulators.

The vitamin D receptor is a transcription factor and member of the steroid hormone nuclear receptor family. It presents a DNA binding domain (VDRE) that, when activated, recruits coregulatory complexes to regulate the genomic activity.

Additionally, ergocalciferol presents nongenomic effects such as the stimulation of intestinal calcium transport via transcaltachia.


The reported LD50 for orally administered ergocalciferol in the rat is of 10 mg/kg. Overdosage with this agent is reported to produce hypervitaminosis characterized by hypercalcemia, renal impairment, calcification of soft tissues, a decline in the rate of linear growth and increase in bone mineralization.

Once an overdose state is registered, immediate withdrawal of vitamin D is required along with a calcium diet, generous intake of fluids and symptomatic treatment. The administration of loop diuretics is an option to increase renal calcium excretion. On the other hand, dialysis and administration of citrates, sulfates, phosphates, corticosteroids, EDTA and mithramycin are recommended.

There haven't been long term studies analyzing the carcinogenic and mutagenic potential of ergocalciferol or its effects in fertility.

Food Interaction

No interactions found.

Volume of Distribution

The amount of circulating ergocalciferol is very limited as this compound is rapidly stored in fat tissue such as adipose tissue, liver and muscle. This is very obvious in reports that indicate that circulating ergocalciferol is significantly reduced in obese patients.

Elimination Route

Ergocalciferol is absorbed in the intestine and carried to the liver in chylomicrons. Its intestinal absorption does not present limitations unless the presence of conditions related to fat malabsorption. However, for absorption to take place, the presence of bile is required.

Half Life

Ergocalciferol can be found circulation for 1-2 days. This quick turnover is presented due to hepatic conversion and uptake by fat and muscle cells where it is transformed to the active form.


There are no formal reports regarding the clearance rate of ergocalciferol. Due to the structural similarity, it is recommended to consult this parameter with cholecalciferol. On the other hand, the proposed renal clearance of calcitriol is of 31 ml/min.

Elimination Route

The active form of ergocalciferol, calcitrol, cannot be maintained for long periods in storage tissue mainly in periods of dietary or UVB deprivation. Therefore, ergocalciferol and its metabolites are excreted via the bile with a minor contribution of renal elimination. This major fecal elimination is explained due to the cubilin-megalin receptor system-mediated renal reuptake of vitamin D metabolites bound to vitamin D binding protein.

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