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Insulin Human

PubChem Reference Collection SID
PubChem CID
Not available because this is not a discrete structure.
Structure
Insulin Human_small.png
Synonyms
  • Insulin Human
  • Human Insulin
  • Insulin (human)
  • Myxredlin
  • Humulin
Description
Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important 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. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. 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. 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. Insulin is typically prescribed later in the course of T2D, after trying 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. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. 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. 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.
Insulin human is an Insulin.
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1 Synonyms

  • Insulin Human
  • Human Insulin
  • Insulin (human)
  • Myxredlin
  • Humulin
  • 1Y17CTI5SR
  • 234-279-7
  • High molecular weight insulin human
  • Insulin Human Regular
  • Insulin human regular (rDNA)
  • Insulin human, rDNA origin
  • Insulin recombinant purified human
  • Insulin, human
  • Regular Insulin, human
  • A10AB01
  • A10AC01
  • A10AD01
  • A10AE01
  • A10AF01
  • CAPSULIN
  • DTXSID7040499
  • EXUBERA (INHALED INSULIN HUMAN)
  • HIGH MOLECULAR WEIGHT INSULIN HUMAN (USP-RS)
  • HUMULIN BR
  • HUMULIN R KWIKPEN
  • Humalog 70/30
  • Humulin R U-100
  • Humulin R U-500
  • Humulin70/30
  • Humulin70/30 KwikPen
  • HumulinN
  • HumulinR
  • HumulinR U-500
  • HumulinR U-500 KwikPen
  • INSULIN HUMAN (USP MONOGRAPH)
  • INSULIN HUMAN (USP-RS)
  • INSULIN HUMAN LENTE
  • INSULIN HUMAN NPH
  • INSULIN HUMAN RDNA
  • INSULIN HUMAN SEMISYNTHETIC
  • INSULIN INJECTION HUMAN BIOSYNTHETIC
  • INSULIN RECONBINANET HUMAN
  • INSULIN SEMI SYNTHETIC HUMAN
  • INSULIN SEMISYNTHETIC HUMAN
  • INSULIN, HUMAN (EP MONOGRAPH)
  • INSULIN,LENTE,HUMAN/RDNA
  • INSULIN,LENTE,HUMAN/SEMISYNTHETIC
  • INSULIN,NPH,HUMAN/RDNA
  • INSULIN,NPH,HUMAN/SEMISYNTHETIC
  • INSULIN,REGULAR,HUMAN BUFFERED
  • INSULIN,REGULAR,HUMAN/RDNA
  • INSULIN,REGULAR,HUMAN/SEMISYNTHETIC
  • INSULIN,ULTRALENTE,HUMAN
  • INSULIN,ULTRALENTE,HUMAN/RDNA
  • Insulin human (rDNA origin)
  • Insulin recombinant
  • Insulina regular
  • Novolin70/30
  • NovolinN
  • NovolinR
  • RPROT P01308 (INS_HUMAN) INSULIN (HGI519)
  • VIATAB
  • human insulin (rDNA)
  • insulin (recombinant)
  • insulin human, for immunoassay
  • insulina umana

2 Structures

2.1 2D Structure

Chemical Structure Depiction
Insulin Human.png

3 Names and Identifiers

3.1 Other Identifiers

3.1.1 CAS

11061-68-0

3.1.2 Deprecated CAS

1021924-27-5, 1038820-20-0, 1104460-98-1, 1146625-72-0, 1171191-96-0, 1171210-94-8, 1171228-96-8, 1171244-30-6, 1245604-13-0

3.1.3 European Community (EC) Number

3.1.4 UNII

3.1.5 DSSTox Substance ID

3.1.6 NCI Thesaurus Code

3.1.7 RXCUI

4 Chemical and Physical Properties

4.1 Experimental Properties

4.1.1 Melting Point

81°C
Khachidze, D.G. et al., J. Biol. Phys. Chem. 1:64-67 (2001)

6 Drug and Medication Information

6.1 Drug Indication

Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus.
Diabetes mellitus where treatment with insulin is required. Insuman Rapid is also suitable for the treatment of hyperglycaemic coma and ketoacidosis, as well as for achieving pre-, intra- and postoperative stabilisation in patients with diabetes mellitus.

6.2 Drug Classes

Breast Feeding; Lactation; Milk, Human; Hypoglycemic Agents

6.3 FDA Approved Drugs

6.4 FDA Purple Book

1 of 4
Application Number
Proper Name
insulin human
Status
Disc; OTC; Rx
Dosage Form
Injection
Route of Administration
Subcutaneous
Product Presentation
Autoinjector; Multi-Dose Vial
BLA Type
351(a)
Licensure
Licensed No. 1891
Date
May 25, 2018; December 29, 2015; October 28, 1982; August 06, 1998; March 31, 1994
Company
Eli Lilly and Company
2 of 4
Application Number
Proper Name
insulin human
Status
OTC
Dosage Form
Injection
Route of Administration
Subcutaneous
Product Presentation
Multi-Dose Vial; Autoinjector
BLA Type
351(a)
Licensure
Licensed No. 1261
Date
June 01, 2018; June 25, 1991
Company
Novo Nordisk Inc.
3 of 4
Application Number
Proper Name
insulin human
Status
Rx
Dosage Form
Powder
Route of Administration
Inhalation
Product Presentation
Single-Dose Cartridge
BLA Type
351(a)
Licensure
Licensed No. 2190
Date
April 17, 2015; June 27, 2014
Company
Mannkind Corporation
4 of 4
Application Number
Proper Name
insulin human
Status
Rx
Dosage Form
Injection
Route of Administration
Intravenous
Product Presentation
Single-Dose Container
BLA Type
351(a)
Licensure
Licensed No. 140
Date
June 20, 2019
Company
Baxter Healthcare Corporation

6.5 FDA National Drug Code Directory

6.6 Drug Labels

Drug and label
Active ingredient and drug

6.7 EMA Drug Information

1 of 13
View All
Medicine
Category
Human drugs
Therapeutic area
Diabetes Mellitus
Active Substance
Insulin human
INN/Common name
insulin human
Pharmacotherapeutic Classes
Drugs used in diabetes
Status
This medicine is authorized for use in the European Union
Company
Sanofi-aventis Deutschland GmbH
Market Date
1997-02-21
2 of 13
View All
Medicine
Category
Human drugs
Therapeutic area
Diabetes Mellitus
Active Substance
Insulin human
INN/Common name
insulin human (rDNA)
Pharmacotherapeutic Classes
Drugs used in diabetes
Status
This medicine is authorized for use in the European Union
Company
Novo Nordisk A/S
Market Date
2002-10-07

7 Pharmacology and Biochemistry

7.1 Pharmacodynamics

Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis).

7.2 FDA Pharmacological Classification

1 of 3
FDA UNII
1Y17CTI5SR
Active Moiety
INSULIN HUMAN
Pharmacological Classes
Chemical Structure [CS] - Insulin
Pharmacological Classes
Established Pharmacologic Class [EPC] - Insulin
FDA Pharmacology Summary
Insulin human is an Insulin.
2 of 3
Non-Proprietary Name
HUMAN INSULIN
Pharmacological Classes
Insulin [EPC]; Insulin [CS]
3 of 3
Non-Proprietary Name
INSULIN HUMAN
Pharmacological Classes
Insulin [EPC]; Insulin [CS]

7.3 ATC Code

A10AB01, A10AC01
A10AC01
A10AB01
A10AD01
QA10AC01
A10AF01
A10AE01

A - Alimentary tract and metabolism

A10 - Drugs used in diabetes

A10A - Insulins and analogues

A10AE - Insulins and analogues for injection, long-acting

A10AE01 - Insulin (human)

A - Alimentary tract and metabolism

A10 - Drugs used in diabetes

A10A - Insulins and analogues

A10AF - Insulins and analogues for inhalation

A10AF01 - Insulin (human)

A - Alimentary tract and metabolism

A10 - Drugs used in diabetes

A10A - Insulins and analogues

A10AB - Insulins and analogues for injection, fast-acting

A10AB01 - Insulin (human)

A - Alimentary tract and metabolism

A10 - Drugs used in diabetes

A10A - Insulins and analogues

A10AC - Insulins and analogues for injection, intermediate-acting

A10AC01 - Insulin (human)

A - Alimentary tract and metabolism

A10 - Drugs used in diabetes

A10A - Insulins and analogues

A10AD - Insulins and analogues for injection, intermediate- or long-acting combined with fast-acting

A10AD01 - Insulin (human)

7.4 Absorption, Distribution and Excretion

Absorption
When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively.
Route of Elimination
Following oral inhalation of human insulin, a mean of 39% of the inhaled dose of carrier particles was distributed to the lungs and a mean of 7% of the dose was swallowed. The swallowed fraction was not absorbed from the GI tract and was eliminated unchanged in the feces.

7.5 Metabolism / Metabolites

The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin.

7.6 Biological Half-Life

Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes.

7.7 Mechanism of Action

The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism.

8 Use and Manufacturing

8.1 Uses

8.1.1 Use Classification

Human drugs -> Drugs used in diabetes -> Human pharmacotherapeutic group -> EMA Drug Category
Veterinary drugs -> Insulins and analogues for injection, intermediate-acting -> Veterinary pharmacotherapeutic group -> EMA Drug Category
Human drugs -> EMA Drug Category

9 Safety and Hazards

9.1 Hazards Identification

9.1.1 GHS Classification

GHS Hazard Statements

Not Classified

Reported as not meeting GHS hazard criteria by 1 of 1 companies. For more detailed information, please visit ECHA C&L website.

9.1.2 Hazard Classes and Categories

Not Classified

10 Toxicity

10.1 Toxicological Information

10.1.1 Effects During Pregnancy and Lactation

◉ Summary of Use during Lactation

Mothers with diabetes using insulin may nurse their infants. Exogenous insulin is excreted into breastmilk, including newer biosynthetic insulins (e.g., aspart, deglutec, detemir, glargine glulisine, lispro). Even direct administration of recombinant insulin orally to preterm infants is safe. Insulin is a normal component of breastmilk and may decrease the risk of type 1 diabetes in breastfed infants. Women taking insulin for type 2 diabetes have higher milk insulin levels than those controlled with diet alone.

Insulin requirements are reduced postpartum in women with type 1 diabetes, although postpartum insulin requirements do not significantly differ between breastfeeding and non-breastfeeding women. In general, insulin requirements are 30% to 50% lower than prepregnancy dosages immediately postpartum. Then the insulin requirements during breastfeeding average 21% lower than prepregnancy dosages, but there is wide variation. In one study, insulin requirements were lower than prepregnancy dosage only during the first week postpartum: 54% of prepregnancy dosage on day 2 and 73% on day 3 postpartum. On day 7 postpartum, insulin dosage returned to prepregnancy requirements. Another study found that dosage requirements did not return to normal for up to 6 weeks in some mothers. A third study found that at 4 months postpartum, patients with type 1 diabetes who exclusively breastfed had an average of 13% lower (range -52% to +40%) insulin requirement than their prepregnancy requirement. A retrospective case-control study found a 34% decrease in postpartum insulin requirement compare to preconception values. There was a nonsignificant trend towards lower requirements in exclusively breastfeeding mothers compared to partial or full formula feeding. A small study found that mothers on insulin pumps were found to have an average basal insulin rates 14% lower and carbohydrate-to-insulin ratios were 10% higher than pre-pregnancy settings. Breastfeeding appears to improve glucose postpartum glucose tolerance in mothers with gestational diabetes mellitus and in normal women.

A small, well-controlled study of women with type 1 diabetes mellitus using continuous subcutaneous insulin found that the average basal insulin requirement in women with type 1 diabetes who breastfed was 0.21 units/kg daily and the total insulin requirement was 0.56 units/kg daily. In similar women who did not breastfeed, the basal insulin requirement was 0.33 units/kg daily and the total insulin requirement was 0.75 units/kg daily. The 36% lower basal insulin requirement was thought to be caused by glucose use for milk production.

Lactation onset occurs later in patients with type 1 diabetes than in women without diabetes, with a greater delay in mothers with poor glucose control. Mothers with type 1 diabetes also discontinue nursing at a higher rate during the first week postpartum. Women with any form of diabetes during pregnancy had more problems with low milk supply than women without diabetes. Once established, lactation persists as long in mothers with diabetes as in mothers without diabetes. However, as in women without diabetes, smoking has a strong negative impact on lactation among mothers with type 1 diabetes. Other factors that have been identified as causes of shorter duration of breastfeeding among type 1 diabetic patients are more frequent caesarean sections and earlier delivery. Among patients with gestational diabetes, those treated with insulin have a delayed onset of lactogenesis II and lower exclusive breastfeeding rates compared to those not treated with insulin.

◉ Effects in Breastfed Infants

Relevant published information was not found as of the revision date. Insulin in breastmilk is thought to be necessary for intestinal maturation of the infant and may help decrease the risk of contracting type 1 diabetes in breastfed infants.

◉ Effects on Lactation and Breastmilk

Proper insulin levels are necessary for lactation. Good glycemic control enhances maternal serum and milk prolactin concentrations and decreases the delay in the establishment of lactation that can occur in mothers with type 1 diabetes.

One-hundred two of 107 consecutive mothers with type 1 diabetes mellitus who delivered were followed at a Danish hospital. Mothers were given prenatal information on breastfeeding and were offered postnatal counseling by a nurse on the benefits of breastfeeding. All infants were admitted to the neonatal intensive care unit at about 2 hours of age for the following 24 hours. When possible, mothers either breastfed or pumped milk for their infants during this time. Mothers were contacted at 5 days and 4 months postpartum to determine their breastfeeding status. The rates of initiation of exclusive and nonexclusive breastfeeding and exclusive formula feeding and the rates at 4 months postpartum were no different from those of the Danish population.

Eight hundred eighty-three women with gestational diabetes were interviewed at 6 to 9 weeks postpartum. Those who had been treated with insulin more frequently reported having a delayed onset of lactogenesis II (>72 hours) postpartum than those not treated with insulin, independent of other maternal risk factors. The odds ratio of having delayed lactogenesis II was 3.1 among insulin-treated mothers compared to mothers with gestational diabetes who did not receive insulin.

A small, controlled trial of women with gestational diabetes compared those treated with insulin to women treated with diet and exercise. Those treated with insulin had a lower rate of exclusive breastfeeding than those treated with diet and exercise (57% vs 81%).

10.1.2 Acute Effects

11 Patents

12 Interactions and Pathways

12.1 Drug-Drug Interactions

13 Information Sources

  1. PubChem Reference Collection
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  3. ChemIDplus
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  11. Drugs and Lactation Database (LactMed)
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  17. NLM RxNorm Terminology
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