Entyvio

Common name: vedolizumab for injection

Trade name: Entyvio

All names: vedolizumab, vedolizumab for injection, vedolizumab, Angio, vedolizumab, Entyvio

[Indications]

Adult ulcerative colitis (UC), adult Crohn's disease[ Crohn's Disease] (CD)

[Dosage]

Recommended dose in UC (ulcerative colitis in adults) and CD (Crohn's disease in adults): 300 mg intravenously over approximately 30 minutes at 0, 2, and 6 weeks and every 8 weeks thereafter.

Entyvio was discontinued in patients who did not show treatment benefit at week 14.

Entyvio lyophilized powder must be reconstituted with sterile water for injection and must be diluted in 250 mL of sterile 0.9% sodium chloride before administration.

Administer infusion solution within 4 hours of reconstitution and dilution.

Give patients all up-to-date immunizations (in accordance with current immunization guidelines) before initiating treatment with Entyvio.

[Adverse Reactions]

The most common adverse reactions (incidence ≥3% and ≥1% higher than placebo): nasopharyngitis, headache, arthritis, nausea, fever, upper respiratory tract infection, fatigue, cough, bronchitis, influenza, back pain, rash, itching, sinusitis, oropharyngeal pain, and limb pain.

[Contraindications]

Entyvio is contraindicated in patients with a known history of severe or severe hypersensitivity reactions (e.g., dyspnea, bronchospasm, urticaria, flushing, rash, and increased heart rate) to Entyvio or any of its excipients.

[Precautions]

Hypersensitivity reactions (including anaphylaxis): If anaphylaxis or other severe allergic reactions occur, discontinue Entyvio.

Infection: It is recommended that patients with active and serious infections not be treated with Entyvio until the infection is controlled. Consider withholding Entyvio in patients who develop serious infections while being treated with Entyvio.

Progressive multifocal leukoencephalopathy: Although no cases were observed in clinical trials of Entyvio, JCV [papillary polyoma vacuolar virus] infection has resulted in progressive multifocal leukoencephalopathy (PML) and death in patients treated with another integrin receptor antagonist. The risks of PML cannot be excluded. Monitor patients for any new or worsening neurological signs and symptoms.

【Storage】

Refrigerate unopened vials at 2° to 8°C (36º to 46ºF). Keep in original packaging to protect from light.

[Mechanism of action]

Vedolizumab is a humanized monoclonal antibody that specifically binds to α4β7 integrin and blocks the interaction between α4β7 integrin and mucosal addressin cell [addressin cell] adhesion molecule-1 (MAdCAM-1) and inhibits the migration of memory T-lymphocytes across the endothelium into the inflamed parenchymal tissue of the gastrointestinal tract. Vedolizumab does not bind to or inhibit the function of α4β1 and αEβ7 integrins and does not antagonize the interaction of α4 integrins with vascular cell adhesion molecule-1 (VCAM-1).

A discrete subset of memory T-lymphocytes that preferentially migrate into the gastrointestinal tract express α4β7 integrin on their surface. MAdCAM-1 is primarily expressed on intestinal endothelial cells and plays a critical role in the homing of T-lymphocytes to intestinal lymphoid tissue. The interaction of α4β7 integrin with MAdCAM-1 contributes significantly to the chronic inflammation that is a hallmark of ulcerative colitis and Crohn's disease.

[Safety and Efficacy]

GEMINI I is a placebo-controlled induction and maintenance study conducted in patients with UC. The results of the study showed that compared with placebo, vedolizumab achieved the primary endpoint of improved clinical response (at 6 weeks of treatment) and clinical remission (at 52 weeks of treatment). In addition, the proportion of patients in the vedolizumab treatment group who achieved mucosal healing (at 6 and 52 weeks of treatment) and glucocorticoid-free clinical remission (at 52 weeks) was significantly higher than that in the placebo group.

GEMINI II is a placebo-controlled induction and maintenance study in patients with CD. The results of the study showed that vedolizumab significantly improved the primary endpoint of clinical remission (at 6 and 52 weeks of treatment) compared with placebo, and the data were statistically significant. At 6 weeks of treatment, there was no significant difference in the co-primary endpoint CDAI-100 response between the vedolizumab and placebo groups. At 52 weeks of treatment, the proportion of patients in the vedolizumab treatment group who achieved CDAI-100 response and glucocorticoid-free clinical remission was significantly higher than that in the placebo group.