Patent 9522163

Prior art

Earlier patents, publications, and products that may anticipate or render the claims unpatentable.

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Prior art

Earlier patents, publications, and products that may anticipate or render the claims unpatentable.

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To identify the most relevant prior art for US patent 9522163, I will search the USPTO database for the patent and examine its cited references.

The following are the prior art references cited in US Patent 9,522,163, along with their details and potential anticipatory relevance:

1. U.S. Patent Documents:

  • US 5,035,236 A

    • Full Citation: US 5,035,236 A (Vaska et al.)
    • Publication/Filing Date: Publication: Jul. 30, 1991; Filing: May 26, 1989.
    • Brief Description: This patent describes a method for treating shock, ischemia, and reperfusion injury using carbon monoxide or carbon monoxide-releasing compounds.
    • Potential Anticipation (35 U.S.C. § 102): This patent potentially anticipates claims related to the use of carbon monoxide for therapeutic purposes, particularly in conditions involving tissue injury or inflammation. While not specifically mentioning "hepatitis," the broad scope of "shock, ischemia, and reperfusion injury" could encompass conditions that lead to or are associated with liver inflammation, a hallmark of hepatitis. For instance, liver ischemia-reperfusion injury can occur during surgery or transplantation, which is a risk factor for hepatitis mentioned in US9522163. Thus, it could potentially anticipate aspects of Claims 1, 11, 13, 15, and 17, depending on the specific wording and scope of "hepatitis" and "treatment" in those claims.

  • US 5,302,634 A

    • Full Citation: US 5,302,634 A (Scholz et al.)
    • Publication/Filing Date: Publication: Apr. 12, 1994; Filing: Apr. 2, 1993.
    • Brief Description: This patent describes compounds and methods for the delivery of nitric oxide (NO) for therapeutic purposes.
    • Potential Anticipation (35 U.S.C. § 102): While this patent focuses on nitric oxide rather than carbon monoxide, it's cited in US9522163, which discusses the interaction between CO, NO, and HO-1 in its mechanism of action for treating hepatitis. If any claims in US9522163 broadly cover the use of gaseous signaling molecules for liver protection or inflammation, this patent might be considered for its general teaching of gas delivery for therapeutic effect. However, it is less directly anticipatory of the core CO-based treatment. It might be relevant as general background art for gas delivery methods described in Claims 11, 13, and 17.

  • US 6,319,956 B1

    • Full Citation: US 6,319,956 B1 (Choi et al.)
    • Publication/Filing Date: Publication: Nov. 20, 2001; Filing: Apr. 20, 2000.
    • Brief Description: This patent (with one of the inventors of US9522163) describes methods and compositions for treating inflammatory disorders using carbon monoxide.
    • Potential Anticipation (35 U.S.C. § 102): This is a highly relevant prior art document as it directly discusses the use of carbon monoxide for inflammatory disorders, and hepatitis is explicitly defined as an inflammatory condition of the liver in US9522163. This patent could potentially anticipate most, if not all, of the independent claims (Claims 1, 11, 13, 15, 17) of US9522163, especially Claim 1 ("treating, preventing, or reducing the risk of, hepatitis in a patient...by administering...carbon monoxide effective to treat hepatitis") and Claim 15 ("treating hepatitis...not caused by surgery and/or endotoxin"). The broad disclosure of using CO for "inflammatory disorders" would likely encompass hepatitis.

  • US 6,346,541 B1

    • Full Citation: US 6,346,541 B1 (Vaska et al.)
    • Publication/Filing Date: Publication: Feb. 12, 2002; Filing: Sep. 28, 2000.
    • Brief Description: This patent is a continuation-in-part of US 5,035,236 and further details methods for treating ischemia-reperfusion injury and shock using carbon monoxide.
    • Potential Anticipation (35 U.S.C. § 102): Similar to US 5,035,236, this patent, being a continuation-in-part, reinforces the prior art knowledge of using CO for conditions related to tissue injury and inflammation. The claims related to treating or preventing hepatitis that might stem from ischemia or reperfusion injury (e.g., in the context of surgery or transplantation, as mentioned in Claim 13) could be anticipated. Therefore, it potentially anticipates aspects of Claims 1, 11, 13, 15, and 17.

2. Other Publications (Non-Patent Literature mentioned in the Description):

  • Verma et al., Science 259:381-384, 1993

    • Full Citation: Verma et al., "Carbon monoxide: a putative neural messenger." Science 259:381-384, 1993.
    • Publication Date: 1993.
    • Brief Description: This publication recognizes carbon monoxide as an important signaling molecule and suggests its role as a neuronal messenger.
    • Potential Anticipation (35 U.S.C. § 102): This reference establishes the general understanding of CO as a biologically active signaling molecule, which forms part of the scientific backdrop for investigating its therapeutic uses. It does not directly anticipate the treatment of hepatitis but provides a foundational understanding that CO has physiological effects.

  • Pozzoli et al., Endocrinology 735:2314-2317, 1994

    • Full Citation: Pozzoli et al., "Carbon monoxide as a neuroendocrine modulator in the hypothalamus." Endocrinology 735:2314-2317, 1994.
    • Publication Date: 1994.
    • Brief Description: This publication suggests carbon monoxide acts as a neuro-endocrine modulator in the hypothalamus.
    • Potential Anticipation (35 U.S.C. § 102): Similar to Verma et al., this reference contributes to the general knowledge of CO's biological activity. It does not directly anticipate the treatment of hepatitis.

  • Utz et al., Biochem Pharmacol. 47:195-201, 1991

    • Full Citation: Utz et al., "Carbon monoxide and nitric oxide: a smooth muscle relaxant system." Biochem Pharmacol. 47:195-201, 1991.
    • Publication Date: 1991.
    • Brief Description: This publication indicates that carbon monoxide is a smooth muscle relaxant, similar to nitric oxide.
    • Potential Anticipation (35 U.S.C. § 102): This reference highlights another known physiological effect of CO. It does not directly anticipate the treatment of hepatitis.

  • Christodoulides et al., Circulation 97:2306-9, 1995

    • Full Citation: Christodoulides et al., "Carbon monoxide is an endogenous vasodilator in vivo." Circulation 97:2306-9, 1995.
    • Publication Date: 1995.
    • Brief Description: This publication discusses carbon monoxide as an endogenous vasodilator.
    • Potential Anticipation (35 U.S.C. § 102): This reference describes CO's role as a vasodilator. It does not directly anticipate the treatment of hepatitis.

  • Mansouri et al., Thromb Haemost. 48:286-8, 1982

    • Full Citation: Mansouri et al., "Carbon monoxide inhibits platelet aggregation." Thromb Haemost. 48:286-8, 1982.
    • Publication Date: 1982.
    • Brief Description: This publication shows that carbon monoxide inhibits platelet aggregation.
    • Potential Anticipation (35 U.S.C. § 102): This reference details another physiological effect of CO. It does not directly anticipate the treatment of hepatitis.

  • Choi et al., Am. J. Respir. Cell Mol. Biol. 15:9-19, 1996

    • Full Citation: Choi et al., "Heme oxygenase-1: a potential target for therapeutic intervention in inflammatory diseases." Am. J. Respir. Cell Mol. Biol. 15:9-19, 1996.
    • Publication Date: 1996.
    • Brief Description: This publication (with one of the inventors of US9522163) discusses heme oxygenase-1 (HO-1) as a potential therapeutic target in inflammatory diseases and lists various inducers of HO-1 expression, including COCl2, endotoxin, and heat shock.
    • Potential Anticipation (35 U.S.C. § 102): This publication is highly relevant as it connects HO-1 induction to inflammatory diseases and lists agents that induce HO-1. Given that US9522163 discusses HO-1 induction in conjunction with CO administration for hepatitis, this reference could be significant for claims that involve combined therapies or the mechanism of action. It directly teaches that HO-1 is a target for inflammatory diseases, and that COCl2 (a CO-releasing compound) and endotoxin can induce HO-1. This could be viewed as relevant to the "inducing HO-1" aspect of claims related to combination therapies (e.g., the embodiment mentioned in the Summary that includes "administering to the patient at least one of the following treatments: inducing HO-1 or ferritin in the patient").

  • Maines, Annu Rev. Pharmacol. Toxicol. 37:517-554, 1997

    • Full Citation: Maines, "The Heme Oxygenase System: A Regulator of Stress Responses and a Target for Therapeutic Intervention." Annu Rev. Pharmacol. Toxicol. 37:517-554, 1997.
    • Publication Date: 1997.
    • Brief Description: This review provides a comprehensive overview of the heme oxygenase system, its role in stress responses, and its potential as a therapeutic target.
    • Potential Anticipation (35 U.S.C. § 102): Similar to Choi et al. (1996), this review article contributes to the general knowledge of HO-1 and its therapeutic potential in inflammatory conditions, which could include hepatitis.

  • Tenhunen et al., J. Lab. Clin. Med. 75:410-421, 1970

    • Full Citation: Tenhunen et al., "Heme oxygenase. Properties of an enzyme system catalyzing the enzymatic conversion of heme to biliverdin." J. Lab. Clin. Med. 75:410-421, 1970.
    • Publication Date: 1970.
    • Brief Description: This publication describes the properties of heme oxygenase, an enzyme involved in heme catabolism.
    • Potential Anticipation (35 U.S.C. § 102): This is a foundational paper on heme oxygenase. It does not directly anticipate the therapeutic use of CO for hepatitis but provides background on the enzyme HO-1, which is part of the mechanism described in US9522163.

  • Keyse et al., Proc. Natl. Acad. Sci. USA 86:99-103, 1989

    • Full Citation: Keyse et al., "Heme oxygenase is induced by oxidative stress in cultured human skin fibroblasts." Proc. Natl. Acad. Sci. USA 86:99-103, 1989.
    • Publication Date: 1989.
    • Brief Description: This publication demonstrates that HO-1 is induced by oxidative stress.
    • Potential Anticipation (35 U.S.C. § 102): This reference contributes to the understanding of HO-1 induction in response to stress. It does not directly anticipate the therapeutic use of CO for hepatitis but is relevant background for the role of HO-1 in cellular responses.

  • Becker-Hapak et al., Methods 24:247-256, 2001

    • Full Citation: Becker-Hapak et al., "Cell-permeable peptides: a new paradigm for drug delivery." Methods 24:247-256, 2001.
    • Publication Date: 2001.
    • Brief Description: This publication describes methods for delivering proteins into cells, such as using TAT-fusion proteins.
    • Potential Anticipation (35 U.S.C. § 102): This reference is cited in US9522163 for methods of delivering exogenous HO-1 protein (e.g., in liposomes or as a TAT-fusion protein). It would be relevant background for any claims related to administering HO-1 protein directly, as an alternative to inducing or expressing it.

  • Sunderman et al., Clin. Chem. 28:2026-2032, 1982

    • Full Citation: Sunderman et al., "Analytical biochemistry of carbon monoxide in blood and breath." Clin. Chem. 28:2026-2032, 1982.
    • Publication Date: 1982.
    • Brief Description: This publication discusses methods for measuring carbon monoxide levels in blood and breath.
    • Potential Anticipation (35 U.S.C. § 102): This reference establishes the prior art for monitoring CO levels, which is a practical consideration for administering CO. This would be relevant to the feasibility of methods described in US9522163 that involve CO administration (Claims 1, 11, 13, 15, 17) and monitoring.

  • Ingi et al., Neuron 16:835-842, 1996

    • Full Citation: Ingi et al., "Carbon monoxide: a novel messenger molecule in the brain." Neuron 16:835-842, 1996.
    • Publication Date: 1996.
    • Brief Description: This publication further explores CO as a messenger molecule in the brain.
    • Potential Anticipation (35 U.S.C. § 102): Similar to Verma et al. and Pozzoli et al., this enhances the general understanding of CO's biological role, but does not directly anticipate the treatment of hepatitis.

  • Morimoto et al., Am. J. Physiol. Heart. Circ. Physiol 280:H482-H488, 2001

    • Full Citation: Morimoto et al., "Detection of sub-ppm carbon monoxide levels in biological tissue by a midinfrared gas sensor." Am. J. Physiol. Heart. Circ. Physiol 280:H482-H488, 2001.
    • Publication Date: 2001.
    • Brief Description: This publication describes a method for detecting sub-ppm carbon monoxide levels in biological tissue.
    • Potential Anticipation (35 U.S.C. § 102): This reference, like Sunderman et al., demonstrates prior art knowledge regarding the measurement and monitoring of CO levels, which supports the practical administration of CO as described in US9522163.

  • Hattler et al., Artif. Organs 18(11):806-812 (1994)

    • Full Citation: Hattler et al., "Oxygenator and catheter for intracorporeal gas exchange." Artif. Organs 18(11):806-812 (1994).
    • Publication Date: 1994.
    • Brief Description: This publication describes an oxygenator and catheter for intracorporeal gas exchange, which could be relevant to delivering gases.
    • Potential Anticipation (35 U.S.C. § 102): This reference provides background on devices for gas delivery, potentially relevant to the "extracorporeal membrane gas exchange device or an artificial lung" mentioned in the description as a method of administration, and thus indirectly to Claim 11, 13, and 17.

  • Golob et al., ASAIO J., 47(5):432-437 (2001)

    • Full Citation: Golob et al., "Intravenous oxygenation via a novel gas-exchange catheter: evaluation in an in vitro model and a small animal model." ASAIO J., 47(5):432-437 (2001).
    • Publication Date: 2001.
    • Brief Description: This publication evaluates an intravenous gas-exchange catheter, another device for gas delivery.
    • Potential Anticipation (35 U.S.C. § 102): Similar to Hattler et al., this reference provides prior art for devices capable of systemic gas delivery, indirectly relevant to methods of administration in Claims 11, 13, and 17.

  • Kim et al., J. Biol. Chem. 272: 1402-1411 (1997)

    • Full Citation: Kim et al., "Inhibition of Fas/APO-1-induced apoptosis by activated ERK/MAP kinase pathway in primary hepatocytes." J. Biol. Chem. 272: 1402-1411 (1997).
    • Publication Date: 1997.
    • Brief Description: This publication describes a method for harvesting mouse primary hepatocytes and discusses TNF-α/ActD treatment to induce cell death (apoptosis) in primary hepatocytes.
    • Potential Anticipation (35 U.S.C. § 102): This reference is cited for experimental methods used in the patent's examples. It does not directly anticipate the therapeutic use of CO for hepatitis but provides context for the in vitro models used to demonstrate the invention.

  • Lowenstein et al. (Proc. Natl. Acad. Sci. U.S.A 90: 9730-9734 (1993))

    • Full Citation: Lowenstein et al., "Nitric oxide-dependent regulation of protein S-nitrosylation in human red blood cells." Proc. Natl. Acad. Sci. U.S.A 90: 9730-9734 (1993).
    • Publication Date: 1993.
    • Brief Description: This publication discusses nitric oxide-dependent regulation. It is cited in US9522163 for methods related to evaluating iNOS expression using a luciferase reporter assay.
    • Potential Anticipation (35 U.S.C. § 102): Similar to Kim et al., this reference is for experimental methodology and does not directly anticipate the therapeutic claims.

  • Taylor et al. (J. Biol. Chem. 273:15148-15156 (1998))

    • Full Citation: Taylor et al., "NF-kappaB activation and nuclear translocation of p65/RelA in human monocytes: effects of lipopolysaccharide and interleukin-1beta." J. Biol. Chem. 273:15148-15156 (1998).
    • Publication Date: 1998.
    • Brief Description: This publication describes methods for electrophoretic mobility shift assay (EMSA) to measure NF-κB nuclear translocation and DNA binding.
    • Potential Anticipation (35 U.S.C. § 102): This reference is for experimental methodology and does not directly anticipate the therapeutic claims.

  • Chow et al. (J. Biol. Chem. 274: 10689-10692 (1999))

    • Full Citation: Chow et al., "Mechanisms of nuclear factor-kappaB activation by endotoxin in mouse peritoneal macrophages." J. Biol. Chem. 274: 10689-10692 (1999).
    • Publication Date: 1999.
    • Brief Description: This publication describes methods for NF-κB activation using a luciferase reporter assay.
    • Potential Anticipation (35 U.S.C. § 102): This reference is for experimental methodology and does not directly anticipate the therapeutic claims.

  • Stenger et al. (J. Exp. Med. 183: 1501-1514 (1996))

    • Full Citation: Stenger et al., "Constitutive and inducible nitric oxide synthase expression in human cerebral cortex." J. Exp. Med. 183: 1501-1514 (1996).
    • Publication Date: 1996.
    • Brief Description: This publication discusses constitutive and inducible nitric oxide synthase expression. It is cited in US9522163 for treating mice with L-NIL in drinking water to inhibit iNOS.
    • Potential Anticipation (35 U.S.C. § 102): This reference provides background on iNOS and methods for its inhibition, which are part of the experimental procedures described in US9522163, but it does not directly anticipate the therapeutic use of CO for hepatitis.

Most Relevant Prior Art:

Based on this analysis, the most relevant prior art documents under 35 U.S.C. § 102 for US Patent 9,522,163 are:

  1. US 6,319,956 B1 (Choi et al.): This patent directly addresses using carbon monoxide to treat inflammatory disorders. Given that hepatitis is an inflammatory disease, this reference has a high likelihood of anticipating the core claims of US9522163 related to treating hepatitis with CO.
  2. US 5,035,236 A (Vaska et al.) and US 6,346,541 B1 (Vaska et al.): These patents disclose the therapeutic use of carbon monoxide for ischemia-reperfusion injury and shock, which can be underlying causes or components of liver injury and inflammation relevant to hepatitis, especially in surgical contexts.
  3. Choi et al., Am. J. Respir. Cell Mol. Biol. 15:9-19, 1996: This non-patent literature directly links HO-1 induction to inflammatory diseases and identifies COCl2 as an HO-1 inducer. This is highly relevant to claims involving HO-1 induction or the mechanism of CO action.

These documents establish that the therapeutic potential of carbon monoxide for inflammatory conditions and specific organ injuries (like ischemia-reperfusion) was known prior to the priority date of US9522163.

Generated 5/29/2026, 9:00:47 PM