Antibodies That Block Tumor Necrosis Factor Alpha (TNFα)
This 2000 patent describes specific human antibodies designed to strongly bind and neutralize a protein called TNFα, which is linked to inflammation and autoimmune diseases.
Original patent title: “Human antibodies that bind human TNFα”
This 2000 patent describes specific human antibodies designed to strongly bind and neutralize a protein called TNFα, which is linked to inflammation and autoimmune diseases. Granted to BASF SE in 2000 with 39 claims and 361 forward citations.
Key facts
Coverage
What does this patent actually cover?
This patent describes specific human antibodies, or parts of them, that are engineered to latch onto a molecule called human tumor necrosis factor alpha (hTNFα). The key is how well and how long they stick: they must bind very tightly (dissociating with a K d of 1x10^-8 M or less) and stay attached for a significant time (dissociating with a K off rate constant of 1x10^-3 s^-1 or less). These binding characteristics allow the antibodies to effectively block the harmful activity of hTNFα, as shown by their ability to neutralize hTNFα's toxicity in lab tests (IC 50 of 1x10^-7 M or less). The patent also details specific sequences for parts of these antibodies, like the CDR3 regions of their light and heavy chains, which are crucial for binding. These antibodies can be used to detect hTNFα or to treat conditions where hTNFα causes problems, such as inflammatory diseases.
The gap
What does this patent NOT cover?
- Antibodies that do not bind human TNFα.
- Antibodies that bind human TNFα but do not meet the specific binding affinity (K d) or dissociation rate (K off) thresholds.
- Antibodies that bind human TNFα but do not neutralize its cytotoxic activity in the specified L929 assay.
- Antibodies that are not human or are not derived from human sequences.
- Antibodies that bind to other molecules besides human TNFα.
These exclusions are unique to PatentBrief — derived from the actual claim language, not patent-office boilerplate.
What made this novel
The inventors precisely defined the required binding characteristics (affinity and dissociation rate) and neutralization potency for human antibodies against TNFα, specifying exact performance metrics and even particular amino acid sequences for critical binding regions.
Schematic visualization of the patent's claim structure. Hand-drawn diagrams in progress for each landmark patent.
Where you've seen this
Real-world examples
Biologic drugs for rheumatoid arthritis
Treatments for Crohn's disease
Therapies for psoriasis
Why it matters
The bigger picture
Tumor Necrosis Factor alpha (TNFα) is a key protein involved in inflammation. When overactive, it contributes to diseases like rheumatoid arthritis, Crohn's disease, and psoriasis. This patent provided a foundational technology for developing highly effective biologic drugs that target and neutralize TNFα, significantly improving treatment options for millions suffering from autoimmune and inflammatory conditions.
Filed
February 9, 1996
Granted
July 18, 2000
Market context
Who's building on this
Companies in this space
BASF SE, the original assigneeassigneeThe entity that owns the patent — usually the inventor's employer or a company.Read more →, was a major player. However, the technology described in this patent became a cornerstone for the development of numerous blockbuster TNFα inhibitor drugs by companies like AbbVie (Humira), Amgen (Enbrel), and Janssen (Remicade), among others.
Market impact
This patent, and the antibodies it describes, was instrumental in the rise of the biologic drug market for autoimmune diseases. It enabled the development of highly effective treatments that offered significant relief for patients, creating a multi-billion dollar therapeutic category and shifting the standard of care for many inflammatory conditions.
Claim 1 — Plain English
What this patent covers
This patent describes specific human antibodies, or parts of them, that are engineered to latch onto a molecule called human tumor necrosis factor alpha (hTNFα). The key is how well and how long they stick: they must bind very tightly (dissociating with a K d of 1x10^-8 M or less) and stay attached for a significant time (dissociating with a K off rate constant of 1x10^-3 s^-1 or less). These binding characteristics allow the antibodies to effectively block the harmful activity of hTNFα, as shown by their ability to neutralize hTNFα's toxicity in lab tests (IC 50 of 1x10^-7 M or less). The patent also details specific sequences for parts of these antibodies, like the CDR3 regions of their light and heavy chains, which are crucial for binding. These antibodies can be used to detect hTNFα or to treat conditions where hTNFα causes problems, such as inflammatory diseases.
The clever bit
The inventors precisely defined the required binding characteristics (affinity and dissociation rate) and neutralization potency for human antibodies against TNFα, specifying exact performance metrics and even particular amino acid sequences for critical binding regions.
What it does not cover
- Antibodies that do not bind human TNFα.
- Antibodies that bind human TNFα but do not meet the specific binding affinity (K d) or dissociation rate (K off) thresholds.
- Antibodies that bind human TNFα but do not neutralize its cytotoxic activity in the specified L929 assay.
- Antibodies that are not human or are not derived from human sequences.
- Antibodies that bind to other molecules besides human TNFα.
Patent timeline
Application submitted to the patent office
Application published, typically 18 months after filing
Patent officially issued
PatentBrief Score
Impact Score
Strong
Citation count
40/40
Highly cited
Claim breadth
20/20
Very broad protection
Recency
0/20
Older than 20 years
Assignee scale
0/20
Independent or smaller assigneeassigneeThe entity that owns the patent — usually the inventor's employer or a company.Read more →
PatentBrief Impact Score — based on citation count, claim breadth, recency, and assignee scale. Not a legal assessment.
Heuristic Value Estimate
What this patent might be worth
$216K – $691K
Midpoint $432K · expired or expiring · industry ×3.0
Heuristic only — blends forward/backward citation counts, claim scope, time remaining, litigation history, and CPC-derived industry baseline. Real valuations need a professional appraisal.
The original legal language
Original claims
39 claims as filed with the patent office.
Concepts involved
Citations
Patent lineage
Cite this patent
Wilton, A. J., Mankovich, J. A., Roberts, A. J., Hoogenboom, H. R. J. M., McGuinness, B. T., White, M., Allen, D. J., Sakorafas, P., Labkovsky, B., Schoenhaut, D., Vaughan, T. J., Salfeld, J. G., & Kaymakcalan, Z. (2000). Antibodies That Block Tumor Necrosis Factor Alpha (TNFα) (U.S. Patent No. 6,090,382). U.S. Patent and Trademark Office. https://patentbrief.org/patent/us/6090382/humira-adalimumab
Auto-generated from the patent record. Double-check author order and the issue date against the official USPTO document before submitting.
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Common Questions
Frequently Asked Questions
What does Antibodies That Block Tumor Necrosis Factor Alpha (TNFα) cover?
This 2000 patent describes specific human antibodies designed to strongly bind and neutralize a protein called TNFα, which is linked to inflammation and autoimmune diseases.
Who owns patent US 6090382?
BASF SE owns this patent, granted in 2000.
When does this patent expire?
This patent has expired and is now in the public domain — anyone can use the invention freely.
What is patent US 6090382 cited by?
This patent has been cited by 361 later patents that build on its ideas.
What problem does this patent solve?
Tumor Necrosis Factor alpha (TNFα) is a key protein involved in inflammation. When overactive, it contributes to diseases like rheumatoid arthritis, Crohn's disease, and psoriasis. This patent provided a foundational technology for developing highly effective biologic drugs that target and neutralize TNFα, significantly improving treatment options for millions suffering from autoimmune and inflammatory conditions.
What does this patent NOT cover?
Antibodies that do not bind human TNFα.
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