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Displaying 654-668 of 1,636 results

1006 Exhibit: Exhibit 1006 707 Patent

Document IPR2016-01343, No. 1006 Exhibit - Exhibit 1006 707 Patent (P.T.A.B. Jul. 1, 2016)
The silver chloride was ?ltered off using a ?ne pore sintered glass ?lter and the precipitate was washed several times with hot water to give a total ?ltrate volume of 100-200 ml.
The resulting potas sium malonate solution was added to the platinum con taining ?ltrate and the mixture was carefully warmed 4,140,707 ~ (to avoid “bumping”) on the hot plate until white crys tals of the product started to form in’ great quantity.
The mixture was stirred on a warm hot plate for 5_—l0 minutes until all the yel low platinum complex had dissolved to give a yellow liquor plus a copious white silver chloride precipitate.
The complex was recrystallized from a minimum volume of boiling water (around 250 mls) with ?ltration through a ?ne pore ?lter prior to cooling to 0° C. Yield of ‘shiny white lea?ets 2.96g (74%).
The solution was re?ltered and the ?ltrate mouse was disected free of superfluous tissue and out under sterile conditions into approximately 10 milli reduced to 20-30 mls in volume and cooled to 0° C. to yield plate yellow crystals (presumably trans gram size pieces.
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1031 Exhibit: Exhibit 1031 Journal of Clinical Oncology directory

Document IPR2016-01343, No. 1031 Exhibit - Exhibit 1031 Journal of Clinical Oncology directory (P.T.A.B. Jul. 1, 2016)
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1134 Exhibit: Email from Krinsky to Lydigsen

Document IPR2016-00318, No. 1134-143 Exhibit - Email from Krinsky to Lydigsen (P.T.A.B. Feb. 14, 2017)
Given that Dr. Chabner and Dr. Zeisel both have very limited availability over the coming weeks, and given each Petitioner’s attendance at the other’s prior depositions, I thought it would be most efficient to offer dates to both Petitioners simultaneously:
We are still working to confirm where Dr. Zeisel will be available on November 30, but it will be in one of Charlotte/Kannapolis, Raleigh/Durham/Chapel Hill, NC, or Washington, DC.
Both Neptune and Sandoz have also requested the deposition of Dr. Clet Niyikiza.
However, as Dr. Niyikiza did not submit affidavit testimony prepared for the proceeding in any of these IPRs, his cross examination is not routine discovery and we do not intend to make him available for deposition.
Best, David M. Krinsky Williams & Connolly LLP 725 Twelfth Street, N.W.
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2068 Exhibit: Exhibit 2068 Refsum

Document IPR2016-00318, No. 2068-37 Exhibit - Exhibit 2068 Refsum (P.T.A.B. Sep. 30, 2016)
In the late 1960s, inborn errors homocysteine metabolism of (homocystinuria) were demon- strated in patients with mental retardation, skeletal abnormali- ties, lens dislocation and prema- ture vascular disease‘.
lts metab- Even moderate homocystein- olism is summarized in Fig. 1. emia may provoke venous throm- The only source of homocys- teine in vertebrates is the hydroly- bosis and premature vascular lesions in the cerebral, peripheral sis of S-adenosylhomocysteine, an and coronary arteries (L. Brati- inhibitor and product of S-aden- strom, Thesis, University of Lund, osylmethionine-dependent trans- 1989).
The fate of intra- cellular homocysteine is either 10 years ago from clinical studies based on measurement of acid- salvage to methionine through soluble mixed disulfides in plasma remethylation, or conversion to cysteine via the trans-sulfuration from a small number of patientsz.
Sec- ondly, lack of homocysteine may trap reduced folate as 5-methyl- tetrahydrofolate because homo- cysteine is the methyl acceptor in the methionine synthase reaction catalysing the conversion of 5-methyltetrahydrofolate to tetra- hydrofolate.
Furthermore, the homocysteine response may re- flect loss of functional cobalamine and folate, and may enhance sen- sitivity towards antifolate drugs such as methotrexate-"‘ (Ermens, A. A. M., PhD Thesis, University of Rotterdam, 1990).
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1102 Exhibit: Teicher 1999

Document IPR2016-00318, No. 1102-111 Exhibit - Teicher 1999 (P.T.A.B. Dec. 22, 2016)
N -[4-[2-(2-AMINO-3,4-dihydro-4-oxo-7H- pyrrolo[2,3 -d]-pyrimidin-5-yl) ethyl]- benzo-yl]-L-glutamic acid, LY231514 (MTA), was discovered through structure activity relationship studies based on the novel antipurine antifolate lometrexol.1 MTA contains a pyrrole moiety in the place of the tetrahydropyridine ring of lome- trexol, which results in a major loss of activity in the inhibition of purine biosynthesis and a shift to the inhibition of pyrimidine biosynthesis (thymi- dylate cycle).2"4 MTA is a substrate for mamma- lian folylpolyglutamate synthase5 and is a potent inhibitor, especially as the triglutamate, of the enzymes thymidylate synthase, dihydrofolate reductase, glycinamide ribonucleotide formyltransferase (GARFF), and aminoimidazole carboxamide ribo- nucleotide formyltransferase.6 In 1984, Jackman et al7 reported that relatively high concentrations of circulating thymidine have been found in human plasma.
Drugs MTA and LY329201 (a GARFT inhibitor) were prepared according to published methods and procedures.2,11,12 Cispla- tin, methotrexate, 5-flt~orouracil, paclitaxel, and doxorubicin were purchased from Sigma Chemical Co (St Louis, MO).
Treatment of HCT 116 tumor-bear- ing animals with MTA and irinotecan resulted in greater than additive tumor growth for the two drugs, reaching 27 days when the iri~otecan dose was 30 mg/kg.
Fractionated radiation therapy was administered locally to the tumor-bearing limb of the nude mice carrying human HCT 116 colon carcinoma xeno- grafts twice daily for 5 days.
Combination treatment regimens including MTA were also used in nude mice bearing subcu- taneously implanted human H460 non-small cell lung carcinoma (Table 1).
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2029 Exhibit: Exhibit 2029 ODwyer

Document IPR2016-00318, No. 2029-9 Exhibit - Exhibit 2029 ODwyer (P.T.A.B. Sep. 30, 2016)
Neither Eli Lilly and Company nor the Publisher assume any responsibility for any injury andlor damage to persons or property arising out of or related to any use of the material contained in this periodical.
The reader is advised to check the appropriate medical literature and the product information currently provided by the manufacturer of each drug to be administered to verify the dosage, the method and dututionof adrriinisttatitm, or contraindications.
A number of phase II studies are completed or ongoing in a wide range of tumor types, and encouraging results have been observed in colorec- tal, breast, non-small cell lung, head and neck, bladder, and cervical cancers.
This study was designed with two stages, with an early stopping rule in the event of poor antitumor activity, and in fact closed after no objective tumor responses were noted in the first 20 patients.
Grade 3 febrile neutropenia was experienced by 12% of patients.” A similar study of MTA in previously untreated non—small cell lung cancer was carried out jointly between Australia and South Africa.
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2103 Exhibit: Exhibit 2103 TX 0330

Document IPR2016-00318, No. 2103-62 Exhibit - Exhibit 2103 TX 0330 (P.T.A.B. Sep. 30, 2016)

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2094 Exhibit: Exhibit 2094 Stabler 1988

Document IPR2016-00318, No. 2094-53 Exhibit - Exhibit 2094 Stabler 1988 (P.T.A.B. Sep. 30, 2016)
Elevation of Total Homocysteine in the Serum of Patients with Cobalamin or Folate Deficiency Detected by capillary Gas Chromatography-Mass spectrometry Sdly P. Sim" Paul D. Ilarcollf Elaine R. Podo|l,' Robert H. Alon.‘ David 6.
For example, the significance of the high incidence of low serum Cbl values in elderly subjects without hematologic abnormalities (5, 6), Address correspondence to Dr. Stablcr, Div.
Some investigators have favored a defect in L-methylmalonyl-CoA mutase as the cause and have sug- gested that the neuropsychiatric abnormalities are due to a buildup in propionyl-CoA and a resultant increase in odd number carbon fatty acids in peripheral nerves and the central nervous system (44-46).
This work was supported by Department of Health and Human Services Research Grants DK2l365 (to Dr. Allen) and DK37l65 (to Dr. Stabler), awarded by the National Institutes of Diabetes and Di- gestive and Kidney Diseases.‘ References 1.
Cobalamin inactivation by nitrous oxide produces severe neurological impairment in fruit bats: protection by methionine and aggravation by folntes Life Sci. 3l:200I-2010.
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2105 Exhibit: Exhibit 2105 TX 2262

Document IPR2016-00318, No. 2105-64 Exhibit - Exhibit 2105 TX 2262 (P.T.A.B. Sep. 30, 2016)

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1111 Exhibit: Lu 1984

Document IPR2016-00318, No. 1111-120 Exhibit - Lu 1984 (P.T.A.B. Dec. 22, 2016)

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1117 Exhibit: Quadros

Document IPR2016-00318, No. 1117-126 Exhibit - Quadros (P.T.A.B. Dec. 22, 2016)

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1109 Exhibit: Cuthbertson and Lloyd

Document IPR2016-00318, No. 1109-118 Exhibit - Cuthbertson and Lloyd (P.T.A.B. Dec. 22, 2016)

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1075 Exhibit: Reply Declaration of Ron Schiff

Document IPR2016-00318, No. 1075-134 Exhibit - Reply Declaration of Ron Schiff (P.T.A.B. Dec. 22, 2016)

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1082 Exhibit: Affidavit and website printouts from Wayback Machine

Document IPR2016-00318, No. 1082-95 Exhibit - Affidavit and website printouts from Wayback Machine (P.T.A.B. Dec. 22, 2016)

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1107 Exhibit: Farber 1947

Document IPR2016-00318, No. 1107-116 Exhibit - Farber 1947 (P.T.A.B. Dec. 22, 2016)

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