Insulin degludec 200units/ml solution for injection 3ml pre-filled disposable devices
Requires a prescription from a doctor or prescriber
Ultralong-acting basal insulin analogue
Safety information for pregnancy and breastfeeding
Pregnancy
Insulin degludec was investigated in studies covering fertility, embryo-fetal development, and pre and post-natal development in rats and during the period of embryo-fetal development in rabbits.
those observed with human insulin, which was probably secondary to maternal hypoglycemia.[L42400]
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Insulin degludec
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Insulin degludec
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
4 branded products available
Part of the Tresiba brand family (generic: Insulin degludec)
MHRA licensed products
View all licensed products for Insulin degludec on the MHRA register
Tresiba FlexTouch 200units/ml solution for injection 3ml pre-filled pens
Tresiba FlexTouch 200units/ml solution for injection 3ml pre-filled pens
Tresiba FlexTouch 200units/ml solution for injection 3ml pre-filled pens
Tresiba FlexTouch 200units/ml solution for injection 3ml pre-filled pens
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
40 unit
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(6)
Type 2 diabetes: insulin degludec (ESNM25)
Type 2 diabetes: insulin degludec/liraglutide (Xultophy) (ESNM60)
Type 1 diabetes in adults: diagnosis and management (NG17)
Type 2 diabetes mellitus in adults: high-strength insulin glargine 300 units/ml (Toujeo) (ESNM65)
Diabetes mellitus type 1 and type 2: insulin glargine biosimilar (Abasaglar) (ESNM64)
Tirzepatide for treating type 2 diabetes (TA924)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 25 · Randomised trials: 25 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
B. Ludvik, F. Giorgino, E. Jódar, et al.
Lancet, 2021
A. Gastaldelli, Kenneth Cusi, L. Fernández Landó, et al.
The lancet. Diabetes & endocrinology, 2022
C. Wysham, A. Bhargava, L. Chaykin, et al.
JAMA, 2017
J. Rosenstock, A. Cheng, R. Ritzel, et al.
Diabetes Care, 2018
Ildiko Lingvay, Marisse Asong, C. Desouza, et al.
JAMA, 2023
- Diabetes Mellitus, Type 2
- Insulin, Long-Acting
- Hypoglycemic Agents
A. Philis-Tsimikas, Marisse Asong, E. Franek, et al.
The lancet. Diabetes & endocrinology, 2023
- Diabetes Mellitus, Type 2
- Hypoglycemia
- Insulin, Long-Acting
D. Russell-Jones, T. Babazono, R. Cailleteau, et al.
Lancet, 2023
- Diabetes Mellitus, Type 1
- Diabetes Mellitus, Type 2
- Hypoglycemia
Gergely Á. Visolyi, B. Domján, Márk M. Svébis, et al.
Canadian journal of diabetes, 2023
- Diabetes Mellitus, Type 2
- Hypoglycemia
- Insulin, Long-Acting
AIMS To compare the efficacy and safety of commercially available fixed ratio combinations (FRC) of glucagon-like peptide 1 receptor agonists (GLP-1RA) and basal insulins by a network meta-analysis (NMA) of randomised controlled trials (RCT) of type 2 diabetes patients. METHODS We report a systematic review and network meta-analyses of RCTs of type 2 diabetes patients randomized to FRCs or to their components for ≥24-weeks reported in PubMed or ClinicalTrials.gov until 28/FEB/2022. Primary outcome was attained HbA1c. Secondary outcomes included fasting plasma glucose, change in body weight, and incident hypoglycaemia. Treatment effects were estimated as mean differences and standard errors (MD; [SE]) or odds ratios (OR) with 95% confidence intervals (95%CI) using iGlarLixi as reference. RESULTS We included 29 RCTs of the 1404 papers identified. No direct comparison between FRCs were found. After excluding some insulin capped trials to reach model consistency, both FRCs were more efficacious regarding HbA1c than their components, however no difference between FRCs were found (MD: -0.10 [SE: 0.10]%). The effect of IDegLira (-0.47 [0.24] mmol/l) and basal insulins was similar to that of iGlarLixi (ref.) on fasting glucose, while GLP-1RA had lower efficacy than iGlarLixi. Weight gain was lower with GLP-1RAs and IDegLira (-0.72 [0.32] kg) than iGlarLixi (ref.) and higher with basal insulins. Incident hypoglycemia (based on different definitions) was least frequent with GLP-1RAs followed by IDegLira (OR 0.78 95%CI 0.39-1.57), iGlarLixi (ref.) and basal insulins. CONCLUSIONS Regarding HbA1c, both FRCs were more efficacious over their individual components with similar efficacies of the two FRCs.
Abstract licence: CC BY
Eman N Alhmoud, M. Saad, N. E. Omar
Frontiers in Endocrinology, 2024
- Diabetes Mellitus, Type 2
- Hypoglycemia
- Insulin, Long-Acting
Raja S, Raja A, Ali A, et al.
2025
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
25 hours
Mechanism
Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein c…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
8 days
Half-life
25 hours
Protein binding
99%
[L42400]…
Volume of distribution
10.6 L
Metabolism
[L42400]
The liver and kidney play the major role in metabolizing insulin.
[A231654]
However,…
Elimination
30 to 80%
[A249935]
Clearance
0.03 L/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Insulin is an essential treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels.[A18561][A18562][A18563][A18564][A174934] As a result, people with T1D rely primarily on exogenous forms of insulin, such as insulin degludec, to lower glucose levels in the blood.[A18561][A18562][A18563][A18564][A174934] Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels.[A18561][A18562][A18563][A18564][A174934] Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells.[A18561][A18562][A18563][A18564][A174934] Insulin is typically prescribed later in the course of T2D, after several oral medications such as DB00331, DB01120, or DB01261 have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own.[A18561][A18562][A18563][A18564][A174934]
Marketed as the brand name product Tresiba, insulin degludec has a duration of action up to 42 hours allowing for once-daily dosing, typically at bedtime.[A18561][A18562][A18563][A18564][A174934] Due to its duration of action, Tresiba is considered "basal insulin" as it provides low concentrations of background insulin that can keep blood sugar stable between meals or overnight.[A18561][A18562][A18563][A18564][A174934] Basal insulin is often combined with short-acting "bolus insulin" such as DB00046, DB01309, or DB01306 to provide higher doses of insulin required following meals. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with the goal of avoiding any periods of hypoglycemia.[A18561][A18562][A18563][A18564][A174934]
Compared to endogenous insulin, insulin degludec has an added hexadecanedioic acid on lysine at the B29 position, allowing for the formation of multi-hexamers.[A18561][A18562][A18563][A18564][A174934] When injected subcutaneously, these multi-hexamers form a drug depot store from which monomers are slowly and continuously absorbed into circulation.[A18561][A18562][A18563][A18564][A174934] As a result, Insulin Degludec has a protracted time action profile due to the delayed absorption from subcutaneous tissue depots into the systemic circulation.[A18561][A18562][A18563][A18564][A174934] Compared to available long-acting analogs such as DB00047 and DB01307, which have a duration of action of 20-24 hours, insulin degludec provides a consistent level of basal insulin over 42 hours with a low peak: trough ratio.[A18561][A18562][A18563][A18564][A174934] Limitations of shorter-acting analogs include more frequent dosing and less stable pharmacokinetics, which may negatively impact patient adherence and glucose control, particularly nocturnal control.[A18561][A18562][A18563][A18564][A174934]
Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst.[A18561][A18562][A18563][A18564][A174934] If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy.[A18561][A18562][A18563][A18564][A174934]
Insulin Degludec was approved by the FDA in September 2015 as the product Tresiba, for use in providing glycemic control to adults with diabetes mellitus.
[L42400]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 792 interactions
More severe episodes of hypoglycemia with coma, seizure, or neurologic impairment may be treated with glucagon for emergency use or concentrated intravenous glucose. After apparent clinical recovery from hypoglycemia, continued observation and additional carbohydrate intake may be necessary to avoid the reoccurrence of hypoglycemia. Hypokalemia must be corrected appropriately.
[L42400]
Insulin degludec was investigated in studies covering fertility, embryo-fetal development, and pre and post-natal development in rats and during the period of embryo-fetal development in rabbits.
Human insulin (NPH insulin) was included as a comparator. In these studies, insulin degludec caused pre and post-implantation losses and visceral/skeletal abnormalities when given subcutaneously at up to 21 U/kg/day in rats and 3.3 U/kg/day in rabbits, resulting in 5 times (rat) and 10 times (rabbit) the human exposure (AUC) at a human subcutaneous dose of 0.75 U/kg/day. Overall, the effects of insulin degludec were similar to
those observed with human insulin, which was probably secondary to maternal hypoglycemia.
[L42400]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L42400]
After the first dose, the median onset of appearance was around one hour. The glucose-lowering effect lasted at least 42 hours after the last of 8 once-daily injections. Insulin degludec concentration reaches steady-state levels after 3-4 days.
[L42400]
[L42400]
[L42400]
The results of the in vitro protein binding studies demonstrate that there is no clinically relevant interaction between insulin degludec and other protein-bound drugs.
[L42400]
[L42560]
[L42400]
The liver and kidney play the major role in metabolizing insulin.
[A231654]
However, while the liver predominantly metabolizes endogenous insulin, exogenous insulin is primarily metabolized due to the kidney since it is not directly delivered into the portal system.
[A231654]
[A249935]
[L42400]
Proteins and enzymes this drug interacts with in the body
Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway, which is responsible for most of the metabolic actions of insulin, and the Ras-MAPK pathway, which regulates expression of some genes and cooperates with the PI3K pathway to control cell growth and differentiation. Binding of the SH2 domains of PI3K to phosphotyrosines on IRS1 leads to the activation of PI3K and the generation of phosphatidylinositol-(3, 4, 5)-triphosphate (PIP3), a lipid second messenger, which activates several PIP3-dependent serine/threonine kinases, such as PDPK1 and subsequently AKT/PKB. The net effect of this pathway is to produce a translocation of the glucose transporter SLC2A4/GLUT4 from cytoplasmic vesicles to the cell membrane to facilitate glucose transport.
Moreover, upon insulin stimulation, activated AKT/PKB is responsible for: anti-apoptotic effect of insulin by inducing phosphorylation of BAD; regulates the expression of gluconeogenic and lipogenic enzymes by controlling the activity of the winged helix or forkhead (FOX) class of transcription factors. Another pathway regulated by PI3K-AKT/PKB activation is mTORC1 signaling pathway which regulates cell growth and metabolism and integrates signals from insulin. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway.
The Ras/RAF/MAP2K/MAPK pathway is mainly involved in mediating cell growth, survival and cellular differentiation of insulin. Phosphorylated IRS1 recruits GRB2/SOS complex, which triggers the activation of the Ras/RAF/MAP2K/MAPK pathway. In addition to binding insulin, the insulin receptor can bind insulin-like growth factors (IGFI and IGFII).
Isoform Short has a higher affinity for IGFII binding. When present in a hybrid receptor with IGF1R, binds IGF1. PubMed:12138094 shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin.
In contrast, PubMed:16831875 shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin. In adipocytes, inhibits lipolysis (By similarity)
IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway.
The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD.
In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins.
In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R.
IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC A10AD06
ATC A10AE56
ATC A10AE06
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Insulin degludec
Additional database identifiers
Drugs Product Database (DPD)
22892
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6091
GenAtlas
INSR
GeneCards
INSR
GenBank Gene Database
M10051
GenBank Protein Database
307070
Guide to Pharmacology
1800
UniProt Accession
INSR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6081
GenAtlas
INS
GeneCards
INS
GenBank Gene Database
AJ009655
UniProt Accession
INS_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5465
GenAtlas
IGF1R
GeneCards
IGF1R
GenBank Gene Database
X04434
GenBank Protein Database
804990
Guide to Pharmacology
1801
UniProt Accession
IGF1R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5381
GenAtlas
IDE
GeneCards
IDE
GenBank Gene Database
M21188
GenBank Protein Database
184556
Guide to Pharmacology
2371
UniProt Accession
IDE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q16252338), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.