1. Dx 88
2. Dx-88
3. Dx-88 Cpd
4. Epi-kal-2
5. Kalbitor
1. Kalbitor
2. Fov2302
3. Dx-88
4. Gtpl6955
| Molecular Weight | 7054 g/mol |
|---|---|
| Molecular Formula | C305H442N88O91S8 |
| XLogP3 | -27.9 |
| Hydrogen Bond Donor Count | 100 |
| Hydrogen Bond Acceptor Count | 110 |
| Rotatable Bond Count | 133 |
| Exact Mass | 7052.0530407 g/mol |
| Monoisotopic Mass | 7049.0429762 g/mol |
| Topological Polar Surface Area | 3120 Ų |
| Heavy Atom Count | 492 |
| Formal Charge | 0 |
| Complexity | 18500 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 60 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 2 | |
|---|---|
| Drug Name | Kalbitor |
| PubMed Health | Ecallantide (Injection) |
| Drug Classes | Immune Modulator |
| Drug Label | KALBITOR (ecallantide) is a human plasma kallikrein inhibitor for injection for subcutaneous use. Ecallantide is a 60-amino-acid protein produced in Pichia pastoris yeast cells by recombinant DNA technology.KALBITOR is a clear and colorless, sterile,... |
| Active Ingredient | Ecallantide |
| Dosage Form | Injectable |
| Route | injection |
| Strength | 10mg/ml |
| Market Status | Prescription |
| Company | Dyax Corp. |
| 2 of 2 | |
|---|---|
| Drug Name | Kalbitor |
| PubMed Health | Ecallantide (Injection) |
| Drug Classes | Immune Modulator |
| Drug Label | KALBITOR (ecallantide) is a human plasma kallikrein inhibitor for injection for subcutaneous use. Ecallantide is a 60-amino-acid protein produced in Pichia pastoris yeast cells by recombinant DNA technology.KALBITOR is a clear and colorless, sterile,... |
| Active Ingredient | Ecallantide |
| Dosage Form | Injectable |
| Route | injection |
| Strength | 10mg/ml |
| Market Status | Prescription |
| Company | Dyax Corp. |
Kalbitor (Ecallantide) is indicated for treatment of acute attacks of hereditary angioedema (HAE) in patients 12 years of age and older. /Included in US product label/
NIH; DailyMed. Current Medication Information for Kalbitor (Ecallantide) Injection, Solution (Revised: September 2014). Available from, as of March 24, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f56aec67-c662-477c-b866-bfc23e8809cf
/BOXED WARNING/ WARNING: ANAPHYLAXIS. Anaphylaxis has been reported after administration of Kalbitor. Because of the risk of anaphylaxis, Kalbitor should only be administered by a healthcare professional with appropriate medical support to manage anaphylaxis and hereditary angioedema. Healthcare professionals should be aware of the similarity of symptoms between hypersensitivity reactions and hereditary angioedema and patients should be monitored closely. Do not administer Kalbitor to patients with known clinical hypersensitivity to Kalbitor.
NIH; DailyMed. Current Medication Information for Kalbitor (Ecallantide) Injection, Solution (Revised: September 2014). Available from, as of March 24, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f56aec67-c662-477c-b866-bfc23e8809cf
Potentially serious hypersensitivity reactions, including anaphylaxis, have occurred in patients treated with Kalbitor. In 255 hereditary angioedema (HAE) patients treated with intravenous or subcutaneous Kalbitor in clinical studies, 10 patients (4%) experienced anaphylaxis. For the subgroup of 187 patients treated with subcutaneous Kalbitor, 5 patients (3%) experienced anaphylaxis. Symptoms associated with these reactions have included chest discomfort, flushing, pharyngeal edema, pruritus, rhinorrhea, sneezing, nasal congestion, throat irritation, urticaria, wheezing, and hypotension. These reactions occurred within the first hour after dosing. Other adverse reactions indicative of hypersensitivity reactions included the following: pruritus (5%), rash (3%), and urticaria (2%). Patients should be observed for an appropriate period of time after administration of Kalbitor, taking into account the time to onset of anaphylaxis seen in clinical trials. Given the similarity in hypersensitivity symptoms and acute HAE symptoms, patients should be monitored closely in the event of a hypersensitivity reaction.
NIH; DailyMed. Current Medication Information for Kalbitor (Ecallantide) Injection, Solution (Revised: September 2014). Available from, as of March 24, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f56aec67-c662-477c-b866-bfc23e8809cf
There are no adequate and well-controlled trials of Kalbitor in pregnant women. Kalbitor has been shown to cause developmental toxicity in rats, but not rabbits. Because animal reproductive studies are not always predictive of human response, Kalbitor should be used during pregnancy only if clearly needed.
NIH; DailyMed. Current Medication Information for Kalbitor (Ecallantide) Injection, Solution (Revised: September 2014). Available from, as of March 24, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f56aec67-c662-477c-b866-bfc23e8809cf
FDA Pregnancy Risk Category: C /RISK CANNOT BE RULED OUT. Adequate, well controlled human studies are lacking, and animal studies have shown risk to the fetus or are lacking as well. There is a chance of fetal harm if the drug is given during pregnancy; but the potential benefits may outweigh the potential risk./
NIH; DailyMed. Current Medication Information for Kalbitor (Ecallantide) Injection, Solution (Revised: September 2014). Available from, as of March 24, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f56aec67-c662-477c-b866-bfc23e8809cf
For more Drug Warnings (Complete) data for Ecallantide (11 total), please visit the HSDB record page.
Indicated for the symptomatic treatment of acute attacks of hereditary angioedema (HAE) in patients 12 years of age and older.
FDA Label
Intravenous administration of ecallantide doses 20 mg/m^2 resulted in prolongation of activated partial thromboplastin time (aPTT) without an indication of bleeding. Ecallantide administration has been associated with instances of arrhythmia. In a clinical trial of patients experiencing acute attacks of hereditary angioedema (HAE), intravenous administration of ecallantide demonstrated a significant improvement in symptoms affecting the oropharynx, abdomen, gastrointestinal tract, and limbs within 4 hours post-administration compared to placebo. A substantial decrease in the severity and duration of attacks was also observed in patients with moderate-to-severe HAE attacks. In clinical trials, ecallantide had no significant effect on the QTc interval, heart rate, or any other components of the ECG.
Analgesics
Compounds capable of relieving pain without the loss of CONSCIOUSNESS. (See all compounds classified as Analgesics.)
Anti-Inflammatory Agents, Non-Steroidal
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. (See all compounds classified as Anti-Inflammatory Agents, Non-Steroidal.)
B - Blood and blood forming organs
B06 - Other hematological agents
B06A - Other hematological agents
B06AC - Drugs used in hereditary angioedema
B06AC03 - Ecallantide
Absorption
Following the administration of a single 30 mg subcutaneous dose of ecallantide in healthy subjects, a mean ( standard deviation) peak plasma concentration (Cmax) of 586 106 ng/mL was achieved. The time to reach Cmax (Tmax) was approximately 2 to 3 hours post-dose. The mean area under the concentration-time curve (AUC) was 3017 402 ng*hr/mL.
Route of Elimination
Ecallantide undergoes renal elimination.
Volume of Distribution
The volume of distribution was 26.4 7.8 L in healthy individuals. Intravenous and subcutaneous administration of ecallantide in patients and in healthy subjects resulted in rapid distribution in the vascular compartment.
Clearance
Plasma clearance was 153 20 mL/min following a single subcutaneous dose of 30 mg ecallantide in healthy subjects. Inter-individual variability in patients and healthy individuals was 38% for clearance.
In a pharmacokinetic study in healthy individuals, peak plasma concentrations of ecallantide were achieved at approximately 2-3 hours following a 30 mg dose of ecallantide administered by subcutaneous injection; an approximate bioavailability of 90% was reported with subcutaneous administration.
American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 3676
Ecallantide is eliminated in urine; however, since the drug is a small protein, metabolic catabolism (or degradation) is also a likely elimination process.
American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 3676
It is not known whether ecallantide is excreted in human milk.
NIH; DailyMed. Current Medication Information for Kalbitor (Ecallantide) Injection, Solution (Revised: September 2014). Available from, as of March 24, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f56aec67-c662-477c-b866-bfc23e8809cf
Ecallantide does not undergo metabolism mediated by the cytochrome P-450 system. No _in vitro_ metabolism studies were performed with ecallantide.
Following subcutaneous administration of 30 mg ecallantide, the mean elimination half-life was 2.0 0.5 hours.
The mean half life of ecallantide is 2 hours.
American Society of Health-System Pharmacists 2015; Drug Information 2015. Bethesda, MD. 2015, p. 3676
The kallikrein-kinin system is a complex proteolytic cascade that promotes inflammatory and coagulation pathways. Human plasma kallikrein acts as a protease to mediate the conversion of High Molecular Weight (HMW) kininogen to bradykinin, which is a vasoactive mediator that increases vascular permeability and induces localized swelling, inflammation, and pain. The actions of kallikrein is regulated by the major endogenous inhibitor, C1-esterase-inhibitor (C1-INH). C1-INH also functions to regulate the activation of the complement and intrinsic coagulation (contact system pathway), which also initiates the production of bradykinin. Upon audoactivation via exposure to negatively charged surfaces, factor XII promotes the generation of factor XIIa and kallikrein. C1-INH inhibits both factor XIIa and kallikrein. Kallikrein may in turn reciprocally activate more FXII. Hereditary angioedema is associated with a deficiency of the C1 inhibitor is caused by a mutation in the C1 INH gene. Resulting effect is excessive production of the vasodilator, bradykinin. The actions of bradykinin produce typical edematous signs and symptoms of hereditary angioedema by enhancing vascular and endothelial permeability, leading to increased outflow of plasma into the interstitium to produce local edema. Ecallantide is a potent, specific and reversible plasma kallikrein inhibitor with an Inhibitory Constant (Ki) of 25 pM. Upon binding to kallikrein and blocking its active site, ecallantide prevents the conversion of HMW kininogen to bradykinin and attenuates the production of bradykinin. By blocking the actions of kallikrein, ecallantide also reduces further activation of fXIIa, halting the positive feedback mechanism leading to more kallikrein production.
Ecallantide, a biosynthetic protein based on the first Kunitz domain of human tissue factor pathway inhibitor, is a reversible and selective inhibitor of plasma kallikrein.
American Society of Health-System Pharmacists 2014; Drug Information 2014. Bethesda, MD. 2014, p. 3675
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