Opdivo vs Tecentriq
Both are checkpoint inhibitors. Here is how Opdivo and Tecentriq compare on class, mechanism, dosing, approval and supply.
At a glance
Key differences
- Same class. Both Opdivo and Tecentriq are checkpoint inhibitors, so they work through the same broad mechanism. Differences between them tend to be about dosing, route, how selective they are, and side effects rather than what they target.
- How they are taken. Both are given by the intravenous route.
- Time on the market. Opdivo was first approved by the FDA in 2014, Tecentriq in 2016. That gives Opdivo roughly 2 more years of real-world use and long-term safety data.
- Who markets them. Opdivo is marketed by Bristol Myers Squibb; Tecentriq by Genentech (Roche).
What each one treats
OPDIVO is a programmed death receptor-1 (PD-1)-blocking antibody indicated for the treatment of: Melanoma • adult and pediatric (12 years and older) patients with unresectable or metastatic melanoma, as a single agent or in combination with ipilimumab. (1.1) • for the adjuvant treatment of adult and pediatric patients 12 years and older with completely resected Stage IIB, Stage IIC, Stage III, or Stage IV melanoma. (1.2) Non-Small Cell Lung Cancer (NSCLC) • adult patients with resectable (tumors ≥4 cm or node positive) non-small cell lung cancer in the neoadjuvant setting, in combination with platinum-doublet chemotherapy. (1.3) • adult patients with resectable (tumors ≥4 cm or node positive) non-small cell lung cancer and no known EGFR mutations or ALK rearrangements, for neoadjuvant treatment, in combination with platinum-doublet chemotherapy, followed by single-agent OPDIVO as adjuva…
TECENTRIQ is a programmed death-ligand 1 (PD-L1) blocking antibody indicated: Non-Small Cell Lung Cancer (NSCLC) as adjuvant treatment following resection and platinum-based chemotherapy for adult patients with Stage II to IIIA NSCLC whose tumors have PD-L1 expression on ≥ 1% of tumor cells, as determined by an FDA-authorized test. ( 1.1 , 14.1 ) for the first-line treatment of adult patients with metastatic NSCLC whose tumors have high PD-L1 expression (PD-L1 stained ≥ 50% of tumor cells [TC ≥ 50%] or PD-L1 stained tumor-infiltrating immune cells [IC] covering ≥ 10% of the tumor area [IC ≥ 10%] ), as determined by an FDA-authorized test, with no EGFR or ALK genomic tumor aberrations. ( 1.1 ) in combination with bevacizumab, paclitaxel, and carboplatin, for the first-line treatment of adult patients with metastatic non-squamous NSCLC with no EGFR or ALK genomic tumor aberrations. ( 1.1 …
How each one works
12.1 Mechanism of Action Binding of the PD-1 ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits T-cell proliferation and cytokine production. Upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors. Nivolumab is a human immunoglobulin G4 (IgG4) monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2, releasing PD-1 pathway-mediated inhibition of the immune response, including the anti-tumor immune response. In syngeneic mouse tumor models, blocking PD-1 activity resulted in decreased tumor growth. Combined nivolumab (ant…
12.1 Mechanism of Action PD L1 may be expressed on tumor cells and/or tumor infiltrating immune cells and can contribute to the inhibition of the anti-tumor immune response in the tumor microenvironment. Binding of PD L1 to the PD 1 and B7.1 receptors found on T cells and antigen presenting cells suppresses cytotoxic T-cell activity, T-cell proliferation and cytokine production. Atezolizumab is a monoclonal antibody that binds to PD L1 and blocks its interactions with both PD 1 and B7.1 receptors. This releases the PD L1/PD 1 mediated inhibition of the immune response, including activation of the anti-tumor immune response without inducing antibody-dependent cellular cytotoxicity. In syngen…
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How this page is built
The facts on this page are pulled directly from official U.S. FDA datasets — they are not written from memory. Each field below names the dataset it came from, so you can check it yourself.
- FDA Drug Label (openFDA) ↗ Indications, mechanism of action and pharmacologic class
- Drugs@FDA ↗ First FDA approval date and the company holding the application
- FDA Drug Shortage Database ↗ Current US supply / shortage status
Plain-English summaries and drug-class explainers are written and reviewed by Sreepriya Prasannan (MSc Digital Transformation of Life Sciences (Innopharma Education / Griffith College); MSc & BSc Botany). Data is retrieved automatically from the sources above and cross-checked with AI-assisted verification (Anthropic's Claude) — brand and generic names are matched against the exact FDA product record so that a combination product or a different formulation cannot be mistaken for the drug on this page. An editor reviews the result before publication. We describe this in full in our editorial standards and corrections policy. The FDA data on this page was last retrieved on 8 Oct 2026. How every register is built: methodology · fixes we have made: corrections log.