DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Status of the Application
Receipt is acknowledged of Applicants’ claims, filed on 04/18/2023, in which claims 1-18 are pending. No preliminary amendment has been filed.
Claims 1-18 are pending and are examined on the merits herein.
Priority
The instant application is a 371 of PCT/US2021/055809, filed on 10/20/2021, which claims domestic benefit to 63/094,032, filed on 10/20/2020.
Information Disclosure Statement
The information disclosure statement (IDS) dated 04/18/2023 complies with the provisions of 37 CFR 1.97, 1.98 and MPEP § 609. Accordingly, the information disclosure statement has been considered by the examiner.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claim(s) 1-2 and 5 are rejected under 35 U.S.C. 102(a)(1) and 35 U.S.C. 102(a)(2) as being anticipated by Huizing, et al. (US 2020/0046747 Al; IDS 04/18/2023).
Huizing discloses a method of treating a subject with a vascular or cardiac disorder associated with oxidative stress (abstract). This method comprises selecting a subject that has the cardiovascular disorder associated with oxidative stress and administering therapeutically effective amount of a mannosamine, N-acetyl mannosamine or a derivative thereof (claim 1). Huizing discloses that the subject has heart failure, atherosclerotic cardiovascular disease, cardiomyopathy, a cardiac arrhythmia, myocardial infarction, ischemic heart disease, stroke, or peripheral arterial disease (claim 2). Huizing discloses administration of about 0.01 to about 2 g of sialyation increasing therapy [0119].
Regarding instant claim 2, it is noted that Huizing does not expressly teach that administration of mannosamine to a subject suffering from an ischemic condition would result in the promotion of endothelial cell proliferation and angiogenesis in the subject, as recited in instant claim 2. However, the instant specification provides example 10 (starting at [0100]) which demonstrates the activity of ManN in a chronic ischemia model that reflects its effects as an endothelial cell mitogen and a pro-angiogenic factor. In this method, mice were orally fed with 20% ManN [0101], resulting in improved blood flow and increased blood vessel densities [0102]. The methods section states that this is 200 µL of 20% ManN solution [0133]. Since the teaching of the prior art suggests administration of a similar amount the same active, mannosamine, to patients of the same patient population, that having the ischemic conditions ischemic heart disease and thrombotic stroke, the result that endothelial cell proliferation and angiogenesis would be promoted would necessarily flow, thereby meeting the instant claim limitations.
Claim(s) 13-14 and 16-18 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Lisanti et al. (EMBO Journal, 1991; PTO-892).
Lisanti discusses the effects of mannosamine on glycosyl phosphatidylinositol (GPI) and GPI-anchored proteins in polarized mammalian cells and in living Trypanosoma brucei. Lisanti teaches that an increasing number of membrane glycoproteins are found anchored to the cell surface via a C-terminal glycophospholipid (GPI; glycosyl-phosphatidylinositol) (page 1969, paragraph 1). Mannosamine treatment biochemically induces a phenotype previously observed only as a consequence of deletion of the C-terminal signal for GPI attachment or a genetic defect in GPI synthesis (page 1975, paragraph 4). Lisanti discloses treatment of T. brucei with 0.5, 1.0, 3.0 and 5.0 mM of mannosamine (Fig. 9).
Lisanti teaches that mannosamine (2-amino-2-deoxy D-mannose) blocks the incorporation of GPI into GPI-anchored proteins. This drastically reduced the surface expression of a GPI-anchored protein in polarized MDCK cells, and converted this apical membrane bound protein to an unpolarized secretory product (abstract). Lisanti discloses experiments in which mannosamine addition transformed the GPI-anchored protein gD-1-DAF into a secretory product (page 1971, paragraph 3 and Figure 7).
Furthermore, mannosamine specifically inhibited the incorporation of the GPI component [3H]ethanolamine into trypanosomal GPI-anchored proteins (abstract). Lisanti discloses experiments in which increasing mannosamine concentration inhibited incorporation of [3H]ethanolamine into PARP, the cell surface GPI-anchored acidic repetitive protein in procyclic T. brucei (Figure 9 and paragraph bridging pages 1973-1974). Lisanti teaches that because mannosamine blocks the synthesis of GPI precursors in Trypanosoma brucei it may prove useful for the treatment of parasitic diseases in which the main parasite coat protein is a GPI anchored protein (paragraph bridging pages 1969-1970).
Regarding instant claim 14, Lisanti discloses administration to Trypanosoma brucei, and thus teaches in vivo administration.
Regarding instant claims 16-18, it is noted that Lisanti does not expressly teach that inhibiting the C-terminal glycosylation of GPI-anchored proteins by GPI would result in stimulating EC proliferation and angiogenesis, as recited in instant claim 16, activating JNK and an unfolded protein response caused by ER stress, as recited in instant claim 17, or inducing changes in N-glycan and O-glycan profiles, as recited in instant claim 18. However, example 10 (starting at [0100]) which demonstrates the activity of ManN in a chronic ischemia model that reflects its effects as an endothelial cell mitogen and a pro-angiogenic factor. In this method, mice were orally fed with 20% ManN [0101], resulting in improved blood flow and increased blood vessel densities [0102]. The methods section states that this is 200 µL of 20% ManN solution [0133]. Furthermore, the examples state that ManN stimulates EC proliferation via both JNK activation and the unfolded protein response caused by ER stress [0067], and Example 1 states that ManN had significant stimulatory effects in the 5-500 µM dose range and was also additive with VEGF in promoting BCEC proliferation [0069]. Furthermore, Example 5 shows the effect of ManN on general protein glycosylation profile, concluding that ManN showed inhibitory activity on N-glycosylation at 400 µM [0084] and an overall decrease in O-glycosylation following treatment with 40 µM ManN [0088].
Since the teaching of the prior art suggests administration of a similar amount of the same active, mannosamine, to cells in a patient for the treatment of parasitic diseases for the same purpose of inhibiting protein glycosylation, the result that stimulating EC proliferation and angiogenesis, activating JNK and an unfolded protein response caused by ER stress, and inducing changes in N-glycan and O-glycan profiles would necessarily flow, thereby meeting the instant claim limitations.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1 and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Huizing (US 2020/0046747 Al; IDS 04/18/2023).
Huizing discloses methods for treating a subject with a vascular or cardiac disorder associated with oxidative stress (abstract). These disorders include, among others, heart failure, atherosclerotic cardiovascular disease, ischemic heart disease [0078], and angina pectoris [0033]. The methods may also be used to treat stroke (claim 2), including thrombotic stroke [0099]. The methods include administering to the subject a therapeutically effective amount of a sialylation increasing therapy, such as a sialic acid precursor, sialic acid, one or more sialylated compounds, mannosamine, or N-acetyl mannosamine or a derivative thereof [0077]. The instant specification defines mannosamine as an N-glycosylation inhibitor (Specification [0086]). Huizing teaches that suitable dosage routes include, among others, intraperitoneal and intravenous routes of administration [0122]. The composition may be administered with other therapeutic agents [0137].
The teachings of Huizing differ from that of the instantly claimed invention in that Huizing does exemplify administration of mannosamine to a subject with an ischemic condition by an intravenous, intraperitoneal, or intravitreal route, as required by instant claim 6.
It would have been prima facie obvious before the effective filing date of the claimed invention to administer the mannosamine of Huizing to a patient with an ischemic disease, such as ischemic heart disease or thrombotic stroke through a intraperitoneal and intravenous routes of administration to arrive at the instantly claimed invention because Huizing teaches administration of mannosamine in sialylation increasing therapy and teaches that sialylation increasing therapy is useful for treating conditions including ischemic heart disease and thrombotic stroke and that suitable dosage forms include intraperitoneal and intravenous routes.
Claim 3 is rejected under 35 U.S.C. 103 as being unpatentable over Huizing (US 2020/0046747 Al; IDS 04/18/2023) as applied to claim 1 above, further in view of Yu et al. (Journal of Neuroscience Research, 1999; PTO-892) and Berthe et al. (Breast Cancer Research and Treatment, 2018; PTO-892).
Huizing teaches the method of claim 1, as discussed in detail above.
The teachings of Huizing differ from that of the instantly claimed invention in that Huizing does not expressly disclose further administering an additional compound that is an N-glycosylation inhibitor, as required by instant claim 3.
Yu discloses that dietary restriction (DR) and 2-deoxyglucose (2-DG) administration reduce focal ischemic brain damage. Yu teaches that stroke is an age-related disorder involving degeneration of neurons resulting from cerebral ischemia. Yu teaches that maintenance of adult rats on a DR regimen resulted in reduced brain damage and improved behavioral outcome in a stroke model. Administration of 2-DG, a nonmetabolizable analogue of glucose also reduced ischemic brain damage and improved behavioral outcome following a model of stroke. 2-DG protected cultured hippocampal neurons against chemical hypoxia, demonstrating a direct protective action on neurons (abstract). Yu teaches that the increased resistance of neurons to ischemic injury conferred by 2-DG is related to increased levels of the stress protein heat-shock protein 70 (HSP-70), a protein previously linked to neuroprotection in cell culture and animal models of excitotoxic and ischemic brain injury (paragraph bridging page 830-831).
Berthe discloses that 2-Deoxyglucose (2-DG), known for its ability to compete with glucose, not only inhibits glycolysis but also N-glycosylation (abstract). Due to the structural similarity of glucose with mannose, 2-DG competes with mannose for the process of N-linked glycosylation of proteins in the endoplasmic reticulum (ER). It is converted in the nucleoside-disphosphate derivative GDP-2-DG, before being incorporated in lipid linked oligosaccharides precursors. The resulting intermediates cannot be further extended by the addition of mannosyl residues, leading to a disruption of glycosylation of proteins. Consequently, misfolded N-glycoproteins accumulate in the ER leading to ER stress and the activation of the unfolded protein response (page 582, paragraph 4).
It would have been prima facie obvious to combine the teachings of Huizing and Yu before the effective filing date of the claimed invention by combining the mannosamine treatment of Huizing with the 2-DG treatment of Yu, which Berthe teaches is an N-glycosylation inhibitor, to arrive at the instantly claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to combine the ischemic stroke treatment of Yu with the method of treating a thrombotic stroke of Huizing because it is prima facie obvious to combine the known prior art elements of ischemic stroke treatments to yield the predictable result of a method of treating ischemic stroke. One of ordinary skill in the art would have a reasonable expectation of success because Huizing teaches that the composition may be administered with other therapeutic agents.
Claim 4 is rejected under 35 U.S.C. 103 as being unpatentable over Huizing (US 2020/0046747 Al; IDS 04/18/2023) as applied to claim 1 above, further in view of Hsieh et al. (US 2021/0379151 A1, PTO-892).
Huizing teaches the method of claim 1, as discussed in detail above.
The teachings of Huizing differ from that of the instantly claimed invention in that Huizing does not expressly disclose further administering VEGF.
Hsieh teaches that VEGF derivatives create a transient window during which the blood brain barrier has enhanced permeability, allowing for entry of therapeutic agents into the brain [0006]. Hsieh discloses a method for delivering a therapeutic agent to the brain of a subject, the method comprising administering a VEGF polypeptide systemically to a subject in need thereof, administering to the subject systemically an effective amount of a therapeutic agent, and then administering a second dose of a VEGF polypeptide (claim 1). Hsieh teaches that the subject may be, among others, a human patient at risk of or suspected of having a brain stroke (claim 17). The term “stroke” may be referred to as ischemic stroke, and includes thrombotic stroke [0107].
It would have been prima facie obvious to combine the teachings of Huizing and Hsieh before the effective filing date of the claimed invention by further administering VEGF in the method of Huizing to patients suffering from thrombotic stroke to arrive at the instantly claimed invention. It would have been prima facie obvious for one of ordinary skill in the art to modify the method of treating thrombotic stroke suggested by Huizing because Hsieh teaches that administration of VEGF creates a transient window during which the blood brain barrier has enhanced permeability, allowing for entry of therapeutic agents into the brain. Thus one of ordinary skill in the art would have been motivated to administer the VEGF of Hsieh to increase the permeability of the blood brain barrier to the mannosamine of Huizing in the treatment of a thrombotic stroke. One of ordinary skill in the art would have a reasonable expectation of success because Huizing teaches that the composition comprising mannosamine may be administered with other therapeutic agents.
Claims 7-8, and 10-12 are rejected under 35 U.S.C. 103 as being unpatentable over Johnson et al. (Journal of Molecular Medicine, 2019; PTO-892), in view of Huizing (US 2020/0046747 Al; IDS 04/18/2023) and Ma et al. (Molecular Medicine Reports, 2019; PTO-892).
Johnson teaches approaches to therapeutic angiogenesis for ischemic heart disease. Angiogenesis is a physiological and pathophysiological process that initiates vascular growth from pre-existing blood vessels in response to a lack of oxygen. Therapeutic angiogenesis has been shown to revascularize ischemic heart tissue, reduce the progression of tissue infarction, and evade the need for invasive surgical procedures or tissue/organ transplants (abstract). Clinical therapy trials for strategies of therapeutic angiogenesis provide outcomes including, among others, improved myocardial viability, cardiac function, and angina frequency (Table 2 on page 145). Johnson further teaches that the combinational method using proteins, genes, and cells has been investigated to enhance the effects observed with monotherapy strategies. Moreover, the combination of cardiovascular disease pharmaceutics with additional growth factors has also been recognized as an alternative strategy for cardiovascular improvement. The combinational method may prove to enhance biological responses, which can translate to beneficial clinical outcomes (paragraph bridging pages 145-146).
Vascular endothelial growth factors (VEGF) are pro-angiogenic cytokines within the circulation (page 142, paragraph 1). The use of proteins or genes to stimulate angiogenesis at the cellular level has been a well-established approach, and VEGF is the most important for the development and differentiation of the vascular network, with favorable preclinical evidence showing significantly increased perfusion, improved tissue metabolism, improved cardiac function, and cardiac protection (paragraph bridging pages 142-143). Clinical trials, such as the Randomized Evaluation of VEGF for Angiogenesis produced minimal results, which may be because virtually all clinical trials have been carried out as monotherapy and could be improved with combinatorial therapy (page 143, paragraph 1).
The teachings of Johnson differ from that of the instantly claimed invention in that Johnson does not teach the administration of mannosamine.
Huizing discloses a method of treating a subject with a vascular or cardiac disorder associated with oxidative stress (abstract). This method comprises selecting a subject that has the cardiovascular disorder associated with oxidative stress and administering therapeutically effective amount of a mannosamine, N-acetyl mannosamine or a derivative thereof (claim 1). Huizing teaches that administration of N-acetyl mannosamine or its derivatives promotes formation of sialic acid [0108]. Huizing discloses that the subject has heart failure, atherosclerotic cardiovascular disease, cardiomyopathy, a cardiac arrhythmia, myocardial infarction, ischemic heart disease, stroke, or peripheral arterial disease (claim 2). Cardiovascular diseases also include, among others, angina pectoris [0033]. Huizing teaches that N-acetyl mannosamine and/or its derivatives, or any sialylation increasing therapeutic agent, may also be used in combination with other therapeutic agents, for example, pain relievers, anti-inflammatory agents, and the like, whether for the conditions described or some other condition [0137]. Huizing teaches that suitable dosage routes include, among others, intraperitoneal and intravenous routes of administration [0122].
Ma discusses methods for treating brain ischemia (abstract), and teaches that cerebroprotein hydrolysate includes brain protein hydrolysate, sialic acid. It protects against cerebral ischemic injury via attenuation of oxidative stress or promotion of angiogenesis (page 3149, paragraph 1). Ma teaches that sialic acid increases blood vessel formation. Ma also teaches that sialic acid interacts with extracellular matrix (ECM) components and growth factors, regulating cell adhesion, migration and proliferation (page 3149, paragraph 1).
One of ordinary skill in the art would have been motivated to administer the combination of mannosamine and VEGF in order to provide therapeutic angiogenesis for ischemic heart disease because Johnson teaches that therapeutic angiogenesis has been shown to revascularize ischemic heart tissue, reduce the progression of tissue infarction, and evade the need for invasive surgical procedures or tissue/organ transplants. One of ordinary skill in the art would have been motivated to administer the mannosamine of Huizing as a combination with the VEGF of Johnson in the treatment of ischemic heart disease in order to enhance the effects observed with VEGF monotherapy, and thus provide beneficial clinical outcomes. One of ordinary skill in the art would have had a reasonable expectation of success because Huizing teaches that mannosamine is a sialylation increasing therapeutic agent, and that administration of N-acetyl mannosamine or its derivatives promotes formation of sialic acid, and Ma teaches that sialic acid increases blood vessel formation. Furthermore, Huizing teaches that mannosamine is suitable for treating ischemic heart disease and may be administered in combination with other agents.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Johnson et al. (Journal of Molecular Medicine, 2019; PTO-892), in view of Huizing (US 2020/0046747 Al; IDS 04/18/2023) and Ma et al. (Molecular Medicine Reports, 2019; PTO-892) as applied to claim 7 above, further in view of Yan Ma et al. (Frontiers in Pharmacology, 2019; PTO-892) and Saunier et al. (The Journal of Biological Chemistry, 1982; PTO-892).
The combined teachings of Johnson, Huizing, and Ma suggest the method of claim 7, as discussed in detail above.
The combined teachings of Johnson, Huizing, and Ma differ from that of the instantly claimed invention in that they do not expressly disclose further administering an additional compound that is an N-glycosylation inhibitor, as required by instant claim 9.
Yan Ma discloses a study of 1-Deoxynojirimycin (DNJ) in patients having coronary heart disease (page 2, paragraph 4). Inclusion criteria require that the patients satisfy the criteria for stable angina pectoris and ischemic heart disease (inclusion criteria, page 3). Patients were administered DNJ, which is a unique polyhydroxy alkaloid that is the main active component in mulberry leaves. DNJ is a potent α-glucosidase inhibitor with strong affinity toward α-glucosidase. DNJ can competitively inhibit the binding of maltoseucrose and other disaccharides to α-glucosidase and prevent the breakdown of disaccharides to form glucose (page 2, paragraph 3). Yan Ma teaches that angina pectoris is the main syndrome of coronary heart disease, and was reduced by DNJ treatment. Thus the study showed that DNJ is a potential drug for stable angina pectoris therapy in coronary heart disease patients (paragraph 6, page 6).
Yan Ma also suggests that DNJ may be considered a complementary treatment (paragraph 6, page 6), and teaches that DNJ improves not only stable angina pectoris symptoms (page 6, paragraph 4), but also anxiety and depression (page 6, paragraph 1), as compared to treatment groups who received only conventional treatment.
Saunier discloses the effect of deoxynojirimycin on intact cells using labeled glycopeptides (abstract). Deoxynojirimycin greatly decreased the proportion of radioactivity present in complex oligosaccharides and rendered high mannose oligosaccharides less susceptible to the action of a-mannosidase. Saunier concludes that deoxynojirimycin inhibits the formation of complex oligosaccharides by interfering with processing glucosidases (abstract). Deoxynojirimycin also inhibited the formation of N-linked complex oligosaccharides in intact cells (page 14160, paragraph 6).
One of ordinary skill in the art would have been motivated to combine the DNJ treatment of coronary heart disease taught by Yan Ma with the method of treating ischemic heart disease comprising administering VEGF and mannosamine suggested by the combined teachings of Johnson, Huizing, and Ma because Yan Ma teaches that DNJ is suitable for treating angina pectoris, a syndrome of coronary heart disease, and Johnson teaches that the combination of cardiovascular disease pharmaceutics with additional growth factors is an alternative strategy for cardiovascular improvement and enhances biological responses, which can translate to beneficial clinical outcomes. One of ordinary skill in the art would have a reasonable expectation of success because the methods suggested by Yan Ma as well as the combined teachings of Johnson, Huizing, and Ma both provide treatment of ischemic heart disease, and Yan Ma teaches that DNJ may be considered a complementary treatment in addition to other treatments of coronary heart disease.
Claims 13 and 15 are rejected under 35 U.S.C. 103 as being unpatentable over Lisanti et al. (EMBO Journal, 1991; PTO-892) in view of Reguera et al. (International Journal for Parasitology: Drugs and Drug Resistance, 2014; PTO-892).
Lisanti discusses the effects of mannosamine on glycosyl phosphatidylinositol (GPI) and GPI-anchored proteins in polarized mammalian cells and in living Trypanosoma brucei. Lisanti teaches that an increasing number of membrane glycoproteins are found anchored to the cell surface via a C-terminal glycophospholipid (GPI; glycosyl-phosphatidylinositol) (page 1969, paragraph 1). Mannosamine treatment biochemically induces a phenotype previously observed only as a consequence of deletion of the C-terminal signal for GPI attachment or a genetic defect in GPI synthesis (page 1975, paragraph 4). Lisanti discloses treatment of T. brucei with 0.5, 1.0, 3.0 and 5.0 mM of mannosamine (Fig. 9).
Lisanti teaches that mannosamine (2-amino-2-deoxy D-mannose) blocks the incorporation of GPI into GPI-anchored proteins. This drastically reduced the surface expression of a GPI-anchored protein in polarized MDCK cells, and converted this apical membrane bound protein to an unpolarized secretory product (abstract). Lisanti discloses experiments in which mannosamine addition transformed the GPI-anchored protein gD-1-DAF into a secretory product (page 1971, paragraph 3 and Figure 7).
Furthermore, mannosamine specifically inhibited the incorporation of the GPI component [3H]ethanolamine into trypanosomal GPI-anchored proteins (abstract). Lisanti discloses experiments in which increasing mannosamine concentration inhibited incorporation of [3H]ethanolamine into PARP, the cell surface GPI-anchored acidic repetitive protein in procyclic T. brucei (Figure 9 and paragraph bridging pages 1973-1974). Lisanti teaches that because mannosamine blocks the synthesis of GPI precursors in Trypanosoma brucei it may prove useful for the treatment of parasitic diseases in which the main parasite coat protein is a GPI anchored protein (paragraph bridging pages 1969-1970).
The teachings of Lisanti differ from that of the instantly claimed invention in that Lisanti does not teach the administration ex vivo.
Reguera discusses the state of the art in methods of drug screening for parasitic infections, further discussing phenotypic screenings for infections by Trypanosoma brucei (page 356, paragraph 3). An exciting approach that is midway between in vitro infections with human THP-1 cells and experimental infections in mice involves using ex vivo explants. Once the infection is established, target-infected organs are harvested in order to develop the ex vivo explant culture. Splenic or lymph node ex vivo infected explants show advantages over in vitro systems, because they include the whole cellular population involved in the host-parasite interaction. In addition, the number of animals used in these trials can be drastically reduced, since a single infected spleen can yield up to four 96-well plates, thus enabling the evaluation of several collections of small molecules at a single dose (page 356, paragraph 4).
One of ordinary skill in the art would have been motivated to administer the mannosamine of Lisanti to the ex vivo model of Reguera in order to test its anti-parasitic activity against Trypanosoma brucei, because Reguera teaches that, as compared to in vivo tests, this method provides the benefit of a decreased number of required animals in trials, as well as providing the whole cellular population involved in the host-parasite interaction, as opposed to in vitro tests. One of ordinary skill in the art would have had a reasonable expectation of success because Lisanti suggests that mannosamine is useful for the treatment of parasitic diseases because of its activity in inhibiting GPI glycosylation and Reguera teaches methods for confirming this efficacy.
Conclusion
No claims are allowed.
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/S.G.H./Examiner, Art Unit 1693
/SCARLETT Y GOON/Supervisory Patent Examiner, Art Unit 1693
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