Details for Patent: 12,171,778

Which drugs does patent 12,171,778 protect, and when does it expire?

Patent 12,171,778 protects RYTELO and is included in one NDA.

This patent has thirty-six patent family members in nineteen countries.

Summary for Patent: 12,171,778

Title:	Methods of treating myelodysplastic syndrome
Abstract:	This disclosure provides methods of treating a myelodysplastic syndrome (MDS) in a subject that is naive to treatment with an agent selected from a hypomethylating agent (HMA) and lenalidomide, or both. The method includes administering to the subject an effective amount of a telomerase inhibitor, such as e.g. imetelstat or imetelstat sodium. In some cases, the subject treated is classified as low or intermediate-1 IPSS risk MDS and/or have MDS relapsed/refractory to Erythropoiesis-Stimulating Agent (ESA).
Inventor(s):	Aleksandra Rizo, Jacqueline Cirillo Bussolari
Assignee:	Geron Corp
Application Number:	US16/047,502
Patent Claim Types: see list of patent claims	Use;

Scope and claims analysis for US Patent 12,171,778 (telomerase inhibitor to treat non-del5q low/intermediate-1 IPSS MDS in treatment-naïve subjects)

US 12,171,778 is a method-of-treatment patent focused on patient selection plus dosing logic for a telomerase inhibitor, with imetelstat explicitly claimed. The claim set is built to narrow infringement risk by requiring (i) MDS risk stratum (low or intermediate-1 IPSS), (ii) non-del5q status, (iii) treatment-naïve status to specified prior drug classes (HMA and/or lenalidomide), and (iv) optional but claim-amplifying clinical sub-criteria (relapsed/refractory, ESA-refractory, transfusion dependence with a units-in-8-weeks threshold). The patent also hard-codes dosing regimens and dose ranges, which can be used both defensively (design around dosing windows) and offensively (argue equivalence less likely for materially different regimens).

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What does US Patent 12,171,778 claim: telomerase inhibitor patient-selection method for MDS?

Core independent claim 1: what must be done and who qualifies

Independent claim 1 requires a sequence:

1. Classify the subject as “naïve to treatment with an agent selected from a hypomethylating agent (HMA), lenalidomide, and combination thereof.”
2. Select the subject for telomerase-inhibitor treatment because the subject was classified as treatment-naïve to that selected agent category.
3. Administer an effective amount of the telomerase inhibitor to treat MDS.

This is a classic method-of-use with diagnostic/prescriptive selection. Infringement hinges on both:

• the pre-treatment classification (the “naïve” designation), and
• the administration of the telomerase inhibitor for that selected patient cohort.

Independent claim 22: same concept but with non-del5q as the selection determinant

Independent claim 22 removes the “naïve to HMA/lenalidomide” element and instead requires:

• classify subject as a non-del5q human subject
• select for telomerase inhibitor because of that classification
• administer effective amount to treat MDS

So claim 22 captures a broader “genotype/cytogenetic selection” strategy. Claim 1 and claim 22 can be read as alternative gating hypotheses for patient selection.

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How narrow are the claim limitations on “treatment-naïve” and which prior therapies trigger non-infringement?

Claim 1’s “naïve” language: HMA, lenalidomide, and combinations

Claim 1’s key phrase is “naïve to treatment with an agent selected from”:

• HMA,
• lenalidomide, and
• combination thereof.

That phrase can be used in two ways operationally:

• If a patient has received any HMA previously, they may fail the “naïve to HMA” requirement for claim 10/12/11-type dependents.
• If a patient has received lenalidomide previously, they may fail the “naïve to lenalidomide” requirement for claim 9/11-type dependents.
• For claim 1 itself, the drafting suggests the classification focuses on the agent category chosen for patient selection. Dependent claims then tighten to specific naïve categories.

Dependents that force specific naïve categories

• Claim 9: naïve to lenalidomide
• Claim 10: naïve to HMA
• Claim 11: naïve to both lenalidomide and HMA
• Claim 12-13: specify HMA as decitabine or azacitidine

Practical infringement consequence: a real-world regimen that uses an HMA or lenalidomide before telomerase inhibition can be argued to fall outside the dependent claim sub-classes, though claim 1’s wording still leaves room for litigation over how “naïve” is assessed when multiple prior-agent categories exist.

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What patents protect imetelstat dosing for MDS in low/intermediate-1 IPSS and non-del5q settings?

Imetelstat is explicitly claimed

• Claim 14: telomerase inhibitor is imetelstat
• Claim 15: imetelstat sodium

So there is no need to establish functional equivalence for the telomerase inhibitor identity for these claim paths.

Claim 16-18: dosing regimens and dose ranges are claim elements

Claim 16 hard-codes multiple cycle/dosing patterns:

• 1–8+ dosage cycles
• each cycle comprising one of these IV regimens:
  • about 7–10 mg/kg once every four weeks
  • about 7–10 mg/kg once weekly for four weeks
  • about 2.5–10 mg/kg once every three weeks
  • about 0.5–9.4 mg/kg once every four weeks

Claim 17-18 narrow further to:

• each cycle: about 7–10 mg/kg q4w
• each cycle: about 7.5 mg/kg q4w

Practical infringement consequence: any commercialization or clinical protocol that uses imetelstat but uses materially different dosing (outside stated “about” ranges, different schedule structure, or non-IV routes) can reduce claim coverage, especially for the dosing-dependent claims (17-18 and 16’s structured cycle options).

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Does US 12,171,778 require low/intermediate-1 IPSS risk and non-del5q?

IPSS limitation exists as a narrowing dependent in claim 4

• Claim 4: low or intermediate-1 IPSS risk MDS

This is tied to claim 1; the “non-del5q” limitation is separately present in claim 7 and claim 8 (and in independent claim 22 and dependents).

Non-del5q is a major restriction

• Claim 7: “non-del5q human patient”
• Claim 8: low/intermediate-1 IPSS and non-del5q
• Claim 21: in the imetelstat context: non-del5q
• Claim 22 independent: non-del5q is the gate

Implication: the patent is materially less likely to cover del5q-positive cohorts unless a court construes “non-del5q” broadly (unlikely given the cytogenetic nature) or unless there are other independent claims not listed here.

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How do the relapsed/refractory and ESA-refractory sub-claims change the scope?

Relapsed/refractory

• Claim 2: relapsed or refractory MDS

• Claim 19 reiterates: relapsed/refractory with low/intermediate-1 IPSS

ESA-refractory

• Claim 3: relapsed/refractory MDS refractory to an erythropoiesis-stimulating agent (ESA)
• Claim 24: same nested ESA-refractory logic
• Claim 35: combines ESA-refractory path with imetelstat and low/intermediate-1 IPSS

These limitations suggest the patent is designed to cover a subset with poorer prior response, which can align with therapeutic sequencing strategies used in practice.

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What does the transfusion dependence threshold mean for infringement risk?

Transfusion dependent is in multiple dependents

• Claim 5: transfusion dependent
• Claim 6: transfusion requirement about 4 units or more during the 8 weeks prior to telomerase inhibitor
• Claim 20: transfusion dependent (in imetelstat context)
• Claim 26 and 27 replicate in the independent claim 22 chain

How this is used tactically

Clinically, transfusion dependence is often operationalized with counts/interval windows. The patent chooses a specific numeric threshold:

• “about 4 units or more”
• “during the 8 weeks prior”

Design-around angle: a competing trial that selects a cohort with lower transfusion burden or uses different selection windows can try to avoid these dependents, though independent claims 1 and 22 (as listed) do not require transfusion dependence.

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Where do the “two independent claim groups” create coverage overlap and how can that matter in litigation?

Coverage overlap map

• Claim 1 group: selection = naïve to HMA and/or lenalidomide categories; telomerase inhibitor administration.
• Claim 22 group: selection = non-del5q; telomerase inhibitor administration.

Shared elements appear in dependents:

• relapsed/refractory status
• ESA-refractory
• low/intermediate-1 IPSS
• transfusion dependence and threshold
• imetelstat identity
• imetelstat sodium
• dosing schedules and ranges

Litigation impact

If an accused infringer argues non-naïve or del5q-positive status, that can knock out portions of claim 1 dependents. Conversely, claim 22 can still be asserted if the accused product targets non-del5q subjects. The dosing-dependent claims can be knocked out by switching schedules or routes.

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How strong is the patent estate for this invention based on claim construction leverage (method selection + product identity + dose)?

Based solely on the claim text provided, the estate strength proxies are:

1. Claiming identity: telomerase inhibitor is explicitly imetelstat/imeteclstat sodium. That reduces enforcement burden on “telomerase inhibitor” interpretation for those claim paths (claims 14-15, 33-34).
2. Claiming patient sub-typing: naïve/ non-del5q/ IPSS risk/ ESA-refractory/ transfusion dependence. These provide factual specificity that can both strengthen enforcement (clear clinical gating) and create litigation leverage for design-around.
3. Claiming dosing structure: cycle-based IV administration with numeric dose ranges and schedule options. This makes “different regimen” a plausible non-infringing alternative if it stays outside “about” ranges and schedule structures.
4. Two independent anchors: claim 1 (treatment naïveties) and claim 22 (non-del5q gating). This reduces the chance that a single factual change eliminates all asserted claim coverage.

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When does US 12,171,778 lose exclusivity for MDS indications: patent expiration and regulatory exclusivity?

No filing date, priority date, or patent-term-adjustment inputs were provided here; therefore a definitive expiration timeline cannot be computed from the information available. The analysis above focuses on claim scope and IP coverage structure rather than absolute calendar dates.

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Orange Book status for US 12,171,778 and FDA listing: what does it imply for generic entry?

No Orange Book listing data, NDA/BLA identifier, or FDA approval pathway details were provided. Without those, the regulatory linkage and Paragraph IV landscape cannot be mapped to specific listing patents.

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Which generic or biosimilar strategies could avoid infringement based on the claim limitations?

Generic entry (small molecule)

Imetelstat is a protein-based therapeutic (oligonucleotide). As framed, US method claims target administration of imetelstat itself. A “generic” manufacturer would still need to avoid:

• telomerase inhibitor administration to the specified selected cohorts, and/or
• the dosing regimens that are tied to dependents.

Design-around approaches inferred from claims

• Cytogenetic selection: avoid treating non-del5q subjects, or ensure clinical labeling and inclusion criteria differ.
• Prior-therapy sequencing: avoid using telomerase inhibitor in populations that are “naïve” to HMA or lenalidomide as those categories are operationalized.
• Dosing schedule: use regimens that are outside the explicit IV schedule options and dose ranges in claim 16 and specifically the 7–10 mg/kg q4w structure in claim 17 or 7.5 mg/kg q4w in claim 18.
• Route: claims specify IV administration; a non-IV route would be an argument against at least the dependent dosing-claims.

These options are litigation-relevant because they map to claim elements rather than mere “difference in effectiveness.”

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How does US 12,171,778 compare with typical imetelstat MDS patent strategies (selection + dosing + biomarkers)?

This patent’s claim architecture aligns with a recurring pattern in oncology patents:

• Patient selection (naïve status or non-del5q genotype)
• Clinical subgroup gating (low/intermediate-1 IPSS, relapsed/refractory, ESA-refractory, transfusion dependence)
• Treatment regimen anchoring (imidetelstat identity plus IV dosing schedule and dose ranges)
• Combination inclusion logic (HMA, lenalidomide, or combinations as the naïve agent category)

Compared with “broad” method claims that only cover “administer telomerase inhibitor to treat MDS,” the dependence on non-del5q and specific dosing options makes this one narrower but more enforceable on fact patterns.

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What patent infringement theories are likely: direct method infringement vs inducement vs contributory?

Under a method-of-treatment claim structure:

• Direct infringement typically arises from prescribing/dispensing/administration in the claimed patient subset with the claimed dosing.
• Induced infringement often becomes the focus when the patent owner can point to clinical protocols, inclusion criteria, and dosing instructions that guide clinicians.
• Contributory infringement depends on the availability of components and knowledge, which would require more data than provided.

The claim text itself supports an enforcement narrative grounded in:

• clinical trial protocols or label-like instructions that implement the selection criteria, and
• product-specific dosing schedules.

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Key claim-by-claim coverage matrix (what each limitation adds)

Claim(s)	Key limiting element(s)	Scope effect
1	MDS treatment; classify subject as naïve to HMA or lenalidomide (or combination); select for telomerase inhibitor; administer	Broadest anchor in provided set for selection based on prior-therapy naïveties
2	relapsed or refractory MDS	narrows to relapsed/refractory
3	relapsed/refractory to ESA	further narrows to ESA-refractory subset
4	low or intermediate-1 IPSS risk	adds risk stratification
5-6	transfusion dependent; ≥ ~4 units in prior 8 weeks	adds operational clinical threshold
7-8	non-del5q; optionally + low/intermediate-1 IPSS	adds cytogenetic exclusion/inclusion gating
9-11	naïve to lenalidomide; naïve to HMA; naïve to both	forces prior therapy status
12-13	HMA is decitabine or azacitidine	forces specific HMA identity
14-15	telomerase inhibitor is imetelstat; imetelstat sodium	anchors to product identity
16-18	dosing cycles and IV schedules with dose ranges; incl. 7–10 mg/kg q4w; 7.5 mg/kg q4w	narrows to regimen; gives design-around handle
19-21	relapsed/refractory + low/intermediate-1; + transfusion dependent; + non-del5q in imetelstat chain	combines multiple clinical gates
22	independent anchor based on non-del5q classification	alternative pathway to cover telomerase inhibitor use without naïve prior-therapy gating
23-24	relapsed/refractory; ESA-refractory	narrows subset
25-27	low/intermediate-1; transfusion dependent with ≥4 units/8 weeks	adds stratification and threshold
28-30	naïve lenalidomide; naïve HMA; naïve both	adds prior-therapy gates within non-del5q anchor
31-32	HMA decitabine or azacitidine	forces HMA identity
33-34	telomerase inhibitor is imetelstat; imetelstat sodium	product identity anchor
35-39	combines non-del5q with relapsed/refractory + low/intermediate-1 and dosing schedules	narrows to very specific fact patterns

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Key Takeaways

• US 12,171,778 is structured around patient selection and regimen specifics, not a broad “treat MDS with telomerase inhibitor” claim.
• Two independent anchors drive enforcement: (i) naïve to HMA/lenalidomide (claim 1 chain) and (ii) non-del5q (claim 22 chain).
• Imetelstat sodium and IV dosing schedules are explicitly claimed, with dose and frequency ranges and cycle-based options (claim 16-18), creating meaningful design-around levers.
• Additional dependents add narrow clinical features: low/intermediate-1 IPSS, relapsed/refractory, ESA-refractory, and transfusion dependence with ≥ ~4 units in prior 8 weeks.

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FAQs

1. If a patient previously received azacitidine, can imetelstat treatment still infringe claim 1?
   Claim 1 depends on “naïve” classification to an HMA/lenalidomide agent category; prior exposure can defeat the naïveties required by claim dependents tied to HMA identity or HMA/lenalidomide naïveties.

2. Does claim 22 cover del5q-positive MDS?
   Claim 22 requires a “non-del5q human subject,” so del5q-positive cohorts do not match that selection element as written.

3. What dosing changes are most likely to fall outside claim 16-18?
   Changes that move outside the stated IV regimen structures and dose ranges for the cycle options (including the specific 7–10 mg/kg q4w pattern in claim 17 and 7.5 mg/kg q4w in claim 18) are most likely to avoid the dosing dependents.

4. Can infringement be avoided by treating ESA-naïve patients instead of ESA-refractory?
   ESA-refractory is a dependent limitation (claims 3 and 24). If ESA-refractory is not met, those dependents do not apply, though independent claims may still apply if their gating elements are satisfied.

5. How does transfusion threshold language affect clinical trial eligibility for enforcement?
   The “about 4 units or more during the 8 weeks prior” is a dependent factual gate; trials that select lower transfusion burdens or use materially different windows can attempt to avoid those dependent claims.

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References

1. United States Patent 12,171,778 (claims as provided in the prompt).

Drugs Protected by US Patent 12,171,778

Applicant	Tradename	Generic Name	Dosage	NDA	Approval Date	TE	Type	RLD	RS	Patent No.	Patent Expiration	Product	Substance	Delist Req.	Patented / Exclusive Use	Submissiondate
Geron	RYTELO	imetelstat sodium	POWDER;INTRAVENOUS	217779-001	Jun 6, 2024		RX	Yes	Yes	12,171,778					TREATMENT OF PATIENTS WITH MYELODYSPLASTIC SYNDROMES (MDS) WITH TRANSFUSION-DEPENDENT ANEMIA
Geron	RYTELO	imetelstat sodium	POWDER;INTRAVENOUS	217779-002	Jun 6, 2024		RX	Yes	Yes	12,171,778					TREATMENT OF PATIENTS WITH MYELODYSPLASTIC SYNDROMES (MDS) WITH TRANSFUSION-DEPENDENT ANEMIA

International Family Members for US Patent 12,171,778

Country	Patent Number	Estimated Expiration	Supplementary Protection Certificate	SPC Country	SPC Expiration
Argentina	112288
Australia	2018307983
Australia	2024219941
Brazil	112020001749