General
Preferred name
desogestrel
Synonyms
Org-2969 ()
Cerazette ()
Desogen ()
Desogestrelum ()
Marvelon-desogestrel ()
Cerazette, Desogen, Desogestrelum, Org-2969 ()
ORG 2969 ()
Feanolla ()
Mircette ()
Zelleta ()
Cerelle ()
Nacrez ()
Desomono ()
Aizea ()
Desogestrel-13C2-d2 ()
P&D ID
PD010112
CAS
54024-22-5
Tags
available
prodrug
drug
Approved by
FDA
First approval
1992
Drug indication
Contraception
Progestin
Drug Status
approved
Max Phase
4.0
Probe control
Probe control not defined
Orthogonal probes
0
No orthogonal probes found
Similar probes
0
No structurally similar probes found
Structure
P&D probe-likeness score
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
ROE
The elimination of desogestrel is found to be mainly renal corresponding to about 6 times the dose eliminated in the bile.[F4127] The elimination of desogestrel is only done as the metabolites and not as the unchanged drug and about 85% of the administered dose can be excreted as metabolites after 6-8 days.[T521]
ABSORPTION
After oral administration, desogestrel is rapidly absorbed and it reaches a peak concentration of 2 ng/ml after 1.5 hours. The bioavailability of desogestrel is reported to be in the range of 60-80% and the reported AUC is of 3000 ng.h/ml.[F4127] Almost all the administered dose is modified to the active metabolite, [etonogestrel].[A176423]
MOA
Desogestrel enters the cell passively and acts by binding selectively to the progesterone receptor and generating low androgenic activity.[T357] Its binding produces an effect like a transcription factor and thus, it produces modifications in the mRNA synthesis.[T34] The active metabolite of desogestrel, [etonogestrel], presents a combination of high progestational activity with minimal intrinsic androgenicity.[FDA label]
INDICATION
Oral desogestrel is used in combination with [ethinylestradiol] as a contraceptive agent for the prevention of pregnancy.[FDA label] Desogestrel is part of the combined oral contraceptives that contain a mix of estrogen and progestin which inhibit ovulation.[L5698]
TOXICITY
Administration of large quantities of desogestrel has been shown to produce strong hormonal effects but to lack chronic toxicity. The reported LD50 in rats after oral administration of desogestrel is higher than 2000 mg/kg.[T521] Overdose hasn't reported serious effects but only symptoms of nausea and withdrawal of bleeding.[FDA label] Most reports haven't linked the administration of desogestrel with the increased risk of breast cancer. The increased risk has been reported to be related to the duration of use. However, several reports indicate a desogestrel-driven increased risk in cervical intra-epithelial neoplasia but the results are still not conclusive.[FDA label]
METABOLISM
Desogestrel is rapidly metabolized in the intestinal mucosa and by first-pass hepatic metabolism[T357] to form the major metabolite of desogestrel is [etonogestrel] which is the biologically active metabolite.[A176333, A176336] This modification is described by the hydroxylation in C3 of the desogestrel molecule.[A176423] Later, etonogestrel is metabolized following the normal pathways of steroid metabolism. On the other hand, due to the 11-methylene side chain, desogestrel cannot be metabolized to other progestins.[F4127]
HALF-LIFE
The terminal half-life of desogestrel is determined to be of 30 hours.[F4127]
MOA
Desogestrel enters the cell passively and acts by binding selectively to the progesterone receptor and generating low androgenic activity.[T357] Its binding produces an effect like a transcription factor and thus, it produces modifications in the mRNA synthesis.[T34]; ; The active metabolite of desogestrel, [etonogestrel], presents a combination of high progestational activity with minimal intrinsic androgenicity.[FDA label]
INDICATION
Oral desogestrel is used in combination with [ethinylestradiol] as a contraceptive agent for the prevention of pregnancy.[FDA label]; ; Desogestrel is part of the combined oral contraceptives that contain a mix of estrogen and progestin which inhibit ovulation.[L5698]
TOXICITY
Administration of large quantities of desogestrel has been shown to produce strong hormonal effects but to lack chronic toxicity. The reported LD50 in rats after oral administration of desogestrel is higher than 2000 mg/kg.[T521] Overdose hasn't reported serious effects but only symptoms of nausea and withdrawal of bleeding.[FDA label]; ; Most reports haven't linked the administration of desogestrel with the increased risk of breast cancer. The increased risk has been reported to be related to the duration of use. However, several reports indicate a desogestrel-driven increased risk in cervical intra-epithelial neoplasia but the results are still not conclusive.[FDA label]
DESCRIPTION
Desogestrel is a progestin (synthetic progesterone-like agent) widely used in third-generation hormonal contraceptives. Desogestrel is converted to (3-ketodesogestrel) in vivo. There has been controversy surrounding reports that third-generation oral contraceptives containing desogestrel pose a risk of dangerous blood clots compared to older second-generation oral contraceptives.
(GtoPdb)
PHARMACODYNAMICS
The effects of desogestrel are divided on reproductive including modification of luteinizing hormone and follicle stimulating hormone, declines on the onset of menstruation, and increases the viscosity of the vaginal fluid; and on metabolic that includes increase insulin secretion and resistance, increased lipase activity, and increased fat deposition.[T34] The effect of desogestrel on the lipids has been studied extensively and the results are contradictory. Desogestrel main therapeutic effect due to its mechanism of action is known to be related to the inhibition of the ovulation in 97% of the cycles. This effect was proven in clinical trials in non-breastfeeding women from which the Pearl failure rate was reported to be of 0.17 per 100 women-years. This result indicated that desogestrel is more efficient when compared to other progestogen-only pills.[A176345] All the therapeutic effect is produced by a transformation of the endometrium followed by an inhibition of the ovulation due to the suppression of other hormones.[T521] Desogestrel has been widely confirmed to be related to an increase in the risk of venous thromboembolism due to the driven increased in blood coagulation factors, leading to a pronounced prothrombotic state.[A176315] However, the effects of desogestrel are known to not impact significantly the level of total cholesterol remaining in the range of change of 10% which allows it to be a molecule that presents a favorable lipid profile.[A176339]
PHARMACODYNAMICS
The effects of desogestrel are divided on reproductive including modification of luteinizing hormone and follicle stimulating hormone, declines on the onset of menstruation, and increases the viscosity of the vaginal fluid; and on metabolic that includes increase insulin secretion and resistance, increased lipase activity, and increased fat deposition.[T34] The effect of desogestrel on the lipids has been studied extensively and the results are contradictory.; ; Desogestrel main therapeutic effect due to its mechanism of action is known to be related to the inhibition of the ovulation in 97% of the cycles. This effect was proven in clinical trials in non-breastfeeding women from which the Pearl failure rate was reported to be of 0.17 per 100 women-years. This result indicated that desogestrel is more efficient when compared to other progestogen-only pills.[A176345] All the therapeutic effect is produced by a transformation of the endometrium followed by an inhibition of the ovulation due to the suppression of other hormones.[T521]; ; Desogestrel has been widely confirmed to be related to an increase in the risk of venous thromboembolism due to the driven increased in blood coagulation factors, leading to a pronounced prothrombotic state.[A176315] However, the effects of desogestrel are known to not impact significantly the level of total cholesterol remaining in the range of change of 10% which allows it to be a molecule that presents a favorable lipid profile.[A176339]
[[ p.pathway_name ]]
[[ compound.targets[tid].gene_name ]]
Compound Sets
19
ChEMBL Approved Drugs
ChEMBL Drugs
Drug Repurposing Hub
DrugBank
DrugBank Approved Drugs
DrugCentral
DrugCentral Approved Drugs
DrugMAP
DrugMAP Approved Drugs
Guide to Pharmacology
LSP-MoA library (Laboratory of Systems Pharmacology)
MedChem Express Bioactive Compound Library
Natural product-based probes and drugs
NCATS Inxight Approved Drugs
NPC Screening Collection
ReFrame library
Selleckchem Bioactive Compound Library
TargetMol Bioactive Compound Library
[[ a.name ]]
[[ ligand_id ]]
free of charge
External IDs
42
Molecular Weight
310.23
Hydrogen Bond Acceptors
1
Hydrogen Bond Donors
1
Rotatable Bonds
1
Ring Count
4
Aromatic Ring Count
0
cLogP
4.87
TPSA
20.23
Fraction CSP3
0.73
Chiral centers
6.0
Largest ring
6.0
QED
0.54
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Pathway
Endocrinology/Hormones
Vitamin D Related/Nuclear Receptor
Target
ER
PR
ESR1, PGR
Progesterone Receptor
Estrogen/progestogen Receptor
Indication
contraceptive
MOA
Progesterone receptor agonist
Biosynthetic Origin
Terpenoid (Steroid)
Therapeutic Indication
Contraception
Therapeutic Class
Hormone Therapy
Contraceptive Agents
Source data
