Patent: 10,130,632

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Summary for Patent: 10,130,632

Title:	Methods for treating renal disease
Abstract:	The invention features methods for treating or reducing the likelihood of developing a renal disease by administering to a subject in need thereof an agent that decreases expression of a pathogenic APOL1. The agents of the method target various signaling pathways and decrease the level of the pathogenic APOL1 polypeptide.
Inventor(s):	Friedman; David J. (Boston, MA), Pollak; Martin R. (Boston, MA)
Assignee:	Beth Israel Deaconess Medical Center, Inc. (Boston, MA)
Application Number:	14/646,055
Patent Claims:	see list of patent claims

Executive summary
US Patent 10,130,632 claims a prevention (and/or reduction in likelihood) method for focal segmental glomerulosclerosis (FSGS) in non-transplant patients selected by APOL1 risk genotypes, using a Janus kinase (JAK) 1/2/3 antagonist. The independent claim is an affinity-and-target constrained method claim (APOL1 genotype-defined patient selection + JAK inhibition), with dependent claims narrowing to specific JAK inhibitors (notably INCB-018424 and CP-690550 and related compounds) and adding testing, ancestry framing, and conventional adjunct therapies (BP agents, steroids, immunosuppressants) including transplant-related steps and ex vivo contact of donor kidney with antagonist.

The patent’s practical enforceability and commercial relevance hinge on (i) whether APOL1 genotype testing was being used in the real-world “identified as being at risk” workflow, (ii) whether the asserted JAK inhibitor regimen is used for FSGS prevention/reduced likelihood rather than treatment of established disease, and (iii) how the claim reads against prior art that already links APOL1 biology to podocyte injury/inflammation pathways and links JAK/STAT modulation to kidney injury. The main litigation/portfolio value is therefore less about covering “any JAK inhibitor for any kidney disease,” and more about capturing the specific genotype-guided prevention setting.

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US Patent 10,130,632 claims: what exactly is protected for APOL1-risk FSGS prevention with JAK1/2/3 antagonists?

Independent claim 1: genotype selection + prevention endpoint + JAK1/2/3 antagonism

Core limitations (all must be met):

1. Patient setting: subject has not had a kidney transplant.
2. Risk identification: subject is identified as at risk based on APOL1 copy-number genotype:
   • two G1 copies, or
   • two G2 copies, or
   • one G1 + one G2.
3. Indication type: treating or reducing likelihood of developing FSGS (prevention/reduced-risk language).
4. Therapeutic mechanism constraint: administer an antagonist of JAK1, JAK2, or JAK3.

This is a method-of-treatment claim with biomarker-driven patient selection and a target class constraint (JAK1/2/3 antagonists).

Dependent claim 2: specified JAK inhibitors (named compounds)

Claim 2 narrows “antagonist” to a defined set including:

• INCB-018424
• TG101348
• WHI-P131
• CP-690550

These map to specific JAK inhibitors used in oncology/autoimmunity development programs (INCB-018424 and TG101348 are commonly associated with JAK2-focused profiles; CP-690550 is a JAK3/JAK1/JAK2-positioned kinase inhibitor class reference).

Dependent claims 3, 19, 20: target specificity (JAK1 vs JAK2 vs JAK3)

• Claim 3: antagonist inhibits JAK1
• Claim 19: antagonist inhibits JAK2
• Claim 20: antagonist inhibits JAK3

These dependent claims create three narrower target lanes within the broader JAK1/2/3 umbrella.

Claims 4 and 18: disease mechanism and biomarker/level effect linkage

• Claim 4: FSGS specifically leads to kidney damage (supports “FSGS is the disease model endpoint” framing).
• Claim 18: administration decreases “level of said polypeptide” relative to a reference subject not administered antagonist.
  • As written, “said polypeptide” is not explicitly specified in the excerpt you provided, but in this type of APOL1-JAK patent, it typically ties to APOL1 (or APOL1-linked polypeptide) or a pathway-relevant marker. This clause can be used to argue functional effect in addition to mechanism.

Claims 5 and 21: APOL1 testing and assay formats

• Claim 5: testing prior to administration for APOL1 allele presence
• Claim 21: testing can be by genomic sequencing, PCR, FISH, or immunoassay

This is important for enforcement because it hooks into the clinical workflow: genotype test steps are claim language. A party that treats without documenting genotype-based selection may have an “induced infringement” defense depending on how the claim is asserted.

Claims 6, 7, 8: genotype- and ancestry-scoped variants

• Claim 6: specifically one G1 + one G2
• Claims 7-8: ancestry language (African/Hispanic, and African-American)
  These additions can help narrow to populations where APOL1 testing is commonly used, but they also create an interpretive question: the independent claim already defines risk by genotype, so ancestry clauses are likely supplementary in claim scope.

Claims 9-11: adjunct therapeutic agent framing (standard-of-care stacking)

Claim 9 allows a further therapeutic agent with Claim 10 and Claim 11 giving long-form examples:

• BP medications (diuretics, alpha blockers, ACE inhibitors, ARBs, calcium channel blockers, vasodilators, renin inhibitor)
• Steroids (corticosteroids)
• Immunosuppressive agents, including:
  • glucocorticoids
  • cytostatics (MMF, FK-506/tacrolimus, azathioprine, cyclophosphamide, methotrexate, etc.)
  • antibodies (anti-CD20, muromonoab-CD3, basiliximab, daclizumab)
  • calcineurin inhibitors and others This is classic “combinations permitted” drafting that helps the patentee capture real-world regimens where JAK inhibitors are layered onto existing nephrology and transplant-adjacent treatments.

Claims 12, 13, 14: transplant workflow and ex vivo donor contact

• Claim 12: after administration of antagonist, transplant donor kidney; prior to transplantation donor kidney contacted with antagonist
• Claim 13: subject in need of a transplant
• Claim 14: after administration transplant donor kidney

These transplant-dependent claims sit awkwardly beside claim 1’s “has not had a kidney transplant” constraint, but they likely cover patients who are pre-transplant (no prior transplant yet) who then receive one after drug administration, including an ex vivo treatment step for the donor organ.

Claim 15: subject is human

A standard dependent narrowing.

Claims 16-17: homozygous genotype variants

• homozygous for G1
• homozygous for G2

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How strong is the patent estate for APOL1-risk FSGS prevention: is this claim novel over JAK kidney inflammation and APOL1 biology?

Patent “strength” driver 1: biomarker-guided patient selection

A key legal and validity leverage point is whether prior art already disclosed:

• identifying APOL1-risk subjects by G1/G2 copy number, and
• using a JAK1/2/3 antagonist to reduce likelihood of FSGS onset.

If either APOL1 genotype selection or JAK-target selection is missing, the independent claim narrows sharply, strengthening novelty. If both are disclosed but under a different indication (eg, treatment of established FSGS rather than prevention), novelty may still be argued via the “reducing likelihood of developing” phrasing.

Patent “strength” driver 2: target-class breadth vs prior art overlap

The independent claim requires antagonism of JAK1/2/3, not a specific compound. That breadth raises validity risk if prior art describes JAK inhibitor effects in kidney injury broadly, but it can still be patentably distinct if the APOL1-genotype-defined prevention setting was not disclosed.

Patent “strength” driver 3: dependent claims name specific inhibitors

Claim 2’s named compounds can be used to:

• support obviousness arguments (if those drugs were known and their use in related diseases suggested)
• but also to establish narrower novelty if prior art did not connect those specific compounds to APOL1-risk FSGS prevention.

Weakness driver: “method of treating/reducing likelihood” can be read broadly

Courts often scrutinize whether a “prevention” claim is functionally supported by clinical or mechanistic evidence. If the field had only treatment signals (not prevention), the “reducing likelihood of developing” may face enablement or obviousness pressure. The presence of testing and a genotype-defined at-risk cohort can help, but only if the specification supports prevention dosing and endpoints.

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What patents protect APOL1-associated FSGS with JAK inhibition in the US besides 10,130,632?

Without the full bibliographic and citation record for US 10,130,632 (publication number, family, assignee, prosecution history, and known forward citations), a comprehensive cross-patent mapping cannot be produced from the claim text alone. The constraint here is that a “patent landscape” requires enumerating specific competing US applications and granted patents, which must be tied to the patent’s official family data and citation graph.

No additional reliable patent list can be generated from the claim excerpt alone.

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Claim-by-claim infringement risk analysis: how would a generic/biosimilar or competitor design around US 10,130,632?

The highest-friction claim elements to avoid

1. APOL1 genotype-defined risk selection (G1/G1, G2/G2, or G1/G2 with two copies total).
   • Design-around: avoid genotype selection in the labeled method.
2. Indication framing as prevention/reduced likelihood of developing FSGS.
   • Design-around: conduct only treatment after FSGS diagnosis, not prevention in at-risk subjects.
3. JAK1/2/3 antagonism.
   • Design-around: use non-JAK pathway drugs (or a JAK inhibitor with an argument it does not “antagonize” the required JAK isoform(s) in a clinically relevant sense).
4. Testing step inclusion (if asserted using dependent claims):
   • Design-around: if a party intentionally omits documented APOL1 testing, it may avoid literal recitation of claim 5/21.
5. Compound selection (if asserted using claim 2):
   • Design-around: use a different JAK inhibitor not in the named list, while still falling within the independent claim’s broader JAK antagonism requirement. This helps only if the asserted claims are limited to claim 2.

How combination therapy language affects design-arounds

Claim 9-11 explicitly permit adding other therapies. That reduces the value of design-arounds based on “we used steroids or ACE inhibitors too,” because those fall within the claim’s allowed adjunct list.

Transplant workflow dependency

Claims 12-14 can be used in transplant contexts where donor kidney ex vivo contact with the antagonist is practiced. Parties avoiding ex vivo donor exposure could narrow away from those dependent claims.

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Orange Book status and FDA regulatory posture of the claimed JAK inhibitors (what does the regulatory pathway imply for enforcement?)

A reliable Orange Book status mapping cannot be generated from the claim excerpt alone. Enforcement against method claims typically turns on:

• whether the drug is marketed/approved for the relevant indication,
• labeling supports the claimed method,
• and whether off-label use is alleged as induced/direct infringement.

No Orange Book listing or approval-date table can be produced without the drug identities and the specific US NDA/BLA entries tied to the named JAK inhibitors.

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Commercial exposure: who would be most at risk if US 10,130,632 is asserted?

Parties likely exposed

• Any company promoting or running clinical programs that use JAK1/2/3 inhibitors in genotype-selected APOL1-risk non-transplanted patients for FSGS prevention or “reducing likelihood of developing” FSGS.
• Any company that includes protocol steps explicitly involving:
  • APOL1 testing (sequencing/PCR/FISH/immunoassay),
  • treatment prior to any FSGS diagnosis,
  • and uses a compound falling within JAK1/2/3 antagonism.

Lower exposure scenarios

• Programs focused on established FSGS treatment after diagnosis may argue they fall outside “reducing likelihood of developing.”
• Programs without APOL1 genotype selection may avoid the patient-identification claim limitations.

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Key takeaways

• US 10,130,632 is a genotype-guided (APOL1) kidney disease prevention method that requires JAK1/2/3 antagonism in non-transplanted at-risk subjects (pre-onset concept).
• The claim’s enforceability is most sensitive to whether real-world and clinical protocol workflows include APOL1 genotype testing and whether the therapeutic goal is prevention/reduced likelihood, not treatment of diagnosed FSGS.
• Dependent claims create additional narrowing around named JAK inhibitors, specific JAK isoform inhibition, assay types, ancestry/genotype subgroups, combination co-therapy, and transplant-related ex vivo donor organ contact.
• A meaningful “landscape” (other US patents, forward citations, litigation posture, Orange Book entries) cannot be enumerated from the claim excerpt alone.

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FAQs

1. How does US 10,130,632 distinguish FSGS prevention from treatment of established disease?
   By claiming “treating or reducing the likelihood of developing FSGS” in subjects identified as at risk prior to disease onset.

2. What patient selection is required by US 10,130,632?
   APOL1 copy-number genotype must show two G1 copies, two G2 copies, or one G1 and one G2.

3. Which steps in the clinical workflow are claim-relevant in US 10,130,632?
   APOL1 testing prior to administration is claimed in a dependent claim, with allowed assay categories including sequencing, PCR, FISH, and immunoassay.

4. Can a competitor avoid infringement by using a JAK inhibitor not named in claim 2?
   It may avoid claim 2 specifically, but not claim 1, which covers any antagonist of JAK1/JAK2/JAK3.

5. Does transplant activity change the risk under US 10,130,632?
   Dependent transplant claims cover scenarios where donor kidneys are contacted with the antagonist prior to transplantation, supporting additional pathways for enforcement in transplant workflows.

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References (APA)

No sources were cited because no bibliographic or external record for US Patent 10,130,632 (assignee, publication number, family, prosecution history, citations, litigation, or FDA regulatory entries) was provided in the prompt.

Details for Patent 10,130,632

Applicant	Tradename	Biologic Ingredient	Dosage Form	BLA	Approval Date	Patent No.	Expiredate
Pharmacia & Upjohn Company Llc	ATGAM	lymphocyte immune globulin, anti-thymocyte globulin (equine)	Injection	103676	December 4, 1996	10,130,632	2033-11-20
Janssen Biotech, Inc.	REMICADE	infliximab	For Injection	103772	August 24, 1998	10,130,632	2033-11-20
Immunex Corporation	ENBREL	etanercept	For Injection	103795	November 2, 1998	10,130,632	2033-11-20
Immunex Corporation	ENBREL	etanercept	For Injection	103795	May 27, 1999	10,130,632	2033-11-20