General
Preferred name
ERGOCALCIFEROL
Synonyms
VD2-D3 ()
Calciferol ()
Ercalciol ()
Vitamin D2 ()
D-Forte ()
NSC-62792 ()
Viosterol ()
Ostelin ()
Viosterol in Oil ()
Oleovitamin D, Synthetic ()
Vitamin D 2 ()
Ergorone ()
Eciferol D2 ()
VITAMIN D ()
Caltrate ()
Oleovitamin D ()
Sterogyl 15H ()
Deltalin ()
Uvesterol D ()
Lanes ()
Sterogyl-15 ()
Ergo-D2 ()
Sterogyl ()
Vitamin d (ergocalciferol) ()
Ergocalciferolum ()
Calciferol In Arach Oil ()
Drisdol ()
Ergoral D2 ()
Osto-D2 ()
P&D ID
PD010199
CAS
50-14-6
31316-19-5
Tags
natural product
drug
available
Approved by
FDA
First approval
1941
Drug Status
nutraceutical
approved
Drug indication
Vitamin (antirachitic)
Hypoparathyroidism
Max Phase
Phase 4
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
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.[T577]
PHARMACODYNAMICS After the activation of the vitamin D receptor, some of the biological changes produced by ergocalciferol include mobilization and accretion of calcium and phosphorus in the bone, absorption of calcium and phosphorus in the intestine, and reabsorption of calcium and phosphorus in the kidney.[T580] ; ; Some other effects known to be produced due to the presence of vitamin D are osteoblast formation, fetus development, induction of pancreatic function, induction of neural function, improvement of immune function, cellular growth and cellular differentiation.[T580]; ; When compared to its vitamin D counterpart [cholecalciferol], ergocalciferol has been shown to present a reduced induction of calcidiol and hence, it is less potent.[A177529]; ; Ergocalciferol supplementation in patients with end-stage renal disease has been shown to generate a significant benefit in lab parameters of bone and mineral metabolism as well as improvement in glycemic control, serum albumin levels and reduced levels of inflammatory markers.[A177526]
MOA 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.[T580]; ; 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.[T580] The target genes in the DNA affected by the presence of ergocalciferol are called vitamin D response elements which are dependent on co-modulators.[A177637]; ; 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.[A177637]; ; Additionally, ergocalciferol presents nongenomic effects such as the stimulation of intestinal calcium transport via transcaltachia.[A177637]
INDICATION Ergocalciferol is indicated for the treatment of hypoparathyroidism, refractory rickets, and familial hypophosphatemia.[FDA label]; ; 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.[L6082]; ; 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.[A177664]; ; 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.[L6085]
ROE The active form of ergocalciferol, calcitrol, cannot be maintained for long periods in storage tissue mainly in periods of dietary or UVB deprivation.[T577] 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.[L6091]
TOXICITY The reported LD50 for orally administered ergocalciferol in the rat is of 10 mg/kg.[MSDS] 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.[L6094]; ; 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.[L6094]; ; There haven't been long term studies analyzing the carcinogenic and mutagenic potential of ergocalciferol or its effects in fertility.
ABSORPTION 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.[T577] However, for absorption to take place, the presence of bile is required.[L6088]
METABOLISM Ergocalciferol is inactive and hence, the first step in the body is ruled by the conversion of this parent compound to 25-hydroxyvitamin D by the action of CYP2R1 followed by the generation of the major circulating metabolite, 1,25-dihydroxyvitamin D or calcitrol.[T577] The generation of this major metabolite is ruled by the activity of CYP27B1 which is a key 1-hydroxylase and CYP24A1 which is responsible for the 25-hydroxylation.[A177637]; ; As part of the minor metabolism, ergocalciferol is transformed into 25-hydroxyvitamin D in the liver by the activity of D-25-hydroxylase and CYP2R1. As well, the formation of 24(R),25dihydroxyvitamin D is performed mainly in the kidneys by the action of 25-(OH)D-1-hydroxylase and 25-(OH)D-24-hydroxylase.[T580]; ; Additionally, there are reports indicating significant activity of 3-epimerase in the metabolism of ergocalciferol which modifies the hydroxy group in C3 from the alpha position to a beta. The epimers formed seemed to have a reduced affinity for the vitamin D plasma proteins and to the vitamin D receptor.[A177637]; ; An alternative activation metabolic pathway has been reported and this process is characterized by the activity of CYP11A1 and its hydroxylation in the C-20. This 20-hydroxylated vitamin D seems to have similar biological activity than calcitriol.[A177637]
Cell lines
0
Organisms
1
Compound Sets
15
Cayman Chemical Bioactives
11791
ChEMBL Approved Drugs
CHEMBL1536
ChEMBL Drugs
CHEMBL1536
Drug Repurposing Hub
DrugBank
DB00153
DrugBank Approved Drugs
DB00153
DrugCentral
2838
DrugCentral Approved Drugs
2838
DrugMAP
DMHO0AR
DrugMAP Approved Drugs
DMHO0AR
MedChem Express Bioactive Compound Library
HY-76542
NCATS Inxight Approved Drugs
VS041H42XC
NPC Screening Collection
Other bioactive compounds
TargetMol Bioactive Compound Library
T1086
External IDs
48
Properties
(calculated by RDKit )
Molecular Weight
396.34
Hydrogen Bond Acceptors
1
Hydrogen Bond Donors
1
Rotatable Bonds
5
Ring Count
3
Aromatic Ring Count
0
cLogP
7.64
TPSA
20.23
Fraction CSP3
0.71
Chiral centers
6.0
Largest ring
6.0
QED
0.47
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Target
VD/VDR
DNA polymerase
VD3
VDR
Endogenous Metabolite
Pathway
Vitamin D Related
DNA Damage/DNA Repair
Metabolism
Metabolic Enzyme/Protease
Vitamin D Related/Nuclear Receptor
Indication
hypoparathyroidism, rickets, hypophosphatemia
Disease Area
endocrinology, orthopedics
MOA
vitamin analog
Therapeutic Class
Vitamins
Source data