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Clinical Data Reported on Vidaza in Hematologic Malignancies and,Advanced Solid Tumors

HDAC Inhibitor MGCD0103 Demonstrates substantial Response Rate in Two Clinical Trials

Clinical Data Presented on Pilot Pharmacokinetic Study of Oral Azacitidine

Exelixis Reports Comprehensive XL880 Phase I Data At ASCO

Exelixis Reports Integrated Data From Phase II Clinical Trials of XL999 at ASCO

Clinical Data Reported on Vidaza in Hematologic Malignancies and Advanced Solid Tumors

Studies Investigating Vidaza in Alternate Dosing Schedules in MDS and in Combination with Valproic Acid for Solid Tumors Presented at the American Society of Clinical Oncology 43rd Annual Meeting

* In alternate dose trial, transfusion independence achieved for 65% to 80% of patients transfusion dependent at baseline

CHICAGO, Ill., June 2, 2007 - Pharmion Corporation (NASDAQ: PHRM) reported today the interim results of several Vidaza (azacitidine for injection) studies in the treatment of hematologic malignancies and advanced solid tumors. These data were presented at the 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO) in Chicago, Ill. (June 1-5, 2007). Pharmion's epigenetic anti-cancer products, which include Vidaza, MCGD0103 and oral Azacitidine, are being investigated in the treatment of hematologic malignancies and solid tumors and are the subject of poster and oral presentations at the Meeting.

"As we continue to evaluate alternative dosing and schedules for Vidaza in MDS, and its potential in solid tumors, we are increasingly impressed with the activity this drug has in multiple tumor types," said Patrick J. Mahaffy, president and CEO of Pharmion. "These studies will help provide us with insight not only into the continuing development of parenteral Vidaza, but, in particular, provide us direction for the development of oral azacitidine."

Tolerability and hematologic improvement assessed using three alternative dosing schedules of azacitidine nal trials and/or larger randomized trials which we expect to commence planning for soon."

"These two studies, which represent surprising single agent activity, as well as a very encouraging combination effect with Vidaza, increase our enthusiasm for epigenetic intervention in cancer and the potential for MGCD0103," said Patrick J. Mahaffy, President and Chief Executive Officer of Pharmion Corporation.

Clinical Trial Details

"A Phase II Study of MGCD0103, a Novel Oral Isotype-Selective Histone Deacetylase (HDAC) Inhibitor in Patients with Relapsed or Refractory Hodgkin Lymphoma" (Abstract #8000, Trial 010). Oral, monotherapy treatment with MGCD0103 demonstrated substantial anti-tumor activity in patients with relapsed or refractory Hodgkin's lymphoma. In this study, patients were given MGCD0103 as a single-agent three times per week for four weeks (one cycle) at a starting dose of 110mg. The objectives of this study are to determine the response and disease control rates, as well as safety, toxicity and pharmacodynamic markers. As of May 2007, 22 patients were enrolled and, of these, 20 were evaluable for response analysis.

All patients enrolled in this study had prior chemotherapy ranging from two to nine prior therapies with the median being four. In addition, 59 percent of enrolled patients had prior radiation treatment and 86 percent had prior autologous bone marrow transplant. Overall, eight patients showed objective responses (two complete responses and six partial responses) and nine experienced stable disease (one patient beyond six months) resulting in a response rate of 40 percent and a disease control rate (CR+PR+SD™ 6 months) of 45 percent in this highly-refractory or relapsed population. In total, 75 percent of patients experienced reduction in tumor size; 60 percent experienced tumor reduction greater than 30 percent. Fifty percent of patients remained on treatment for four or more cycles.

Fatigue and gastrointe stinal side effects were the most common adverse effects and dose modification was effective in many of these patients. HDAC inhibition of 20 percent or more was demonstrated in 78 percent of the eleven patients tested. Subsequent studies, expected to be disclosed later this year, are planned, including consideration of registrational opportunities as a single-agent and/or in combination with other agents in this patient population. Enrollment continues and treatment is ongoing in five patients. This trial is expected to complete enrollment by the end of this year.

"A Phase I/II Study of the Oral Isotype-Selective Histone Deacetylase (HDAC) Inhibitor MGCD0103 in Combination with Azacitidine in Patients with High-Risk Myelodysplastic Syndrome (MDS) or Acute Myelogenous Leukemia (AML)" (Abstract #7062, Trial 005). The objectives of this study include determining response rates, maximum tolerated dose, safety, tolerability, pharmacokinetics and the degree of inhibition of the target enzyme.

A total of 37 patients were evaluated for activity and 30 of these patients received doses for which clinical activity had previously been documented (MGCD0103 doses of 60mg, 90mg and 110mg). Seventy-eight percent of patients, with their median age being 67 years, had prior chemotherapy. Eleven patients experienced objective clinical responses resulting in a 30 percent response rate for all patients, and a 37 percent response rate in the active dose ranges previously reported. Six of the 11 responders are continuing treatment, with their mean duration on study being about five cycles (approximately five months). Nine responses were seen in AML patients and two in MDS patients. Dose-limiting toxicities were gastrointestinal in nature. The maximum tolerated dose (MTD) was initially determined to be 110mg; however, upon patient treatment expansion at this dose, the MTD was re-evaluated and enrollment continued at starting doses of 90mg three times per week, with Vidaza do sed as labeled. Pharmacokinetic data for the two agents in combination is similar to either drug alone. The responses are summarized as: five complete responses (CR), five complete responses with incomplete peripheral count recovery (CR-i) and one partial response (PR). Significant HDAC activity inhibition was seen in most patients.

Enrollment is ongoing and expected to be complete by year end. Subsequent studies are planned including potentially larger randomized trials in either or both patient populations (MDS and AML).

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About Hodgkin's Lymphoma

Hodgkin's lymphoma (HL) is a cancer of the lymphatic system that begins in the lymph nodes and progresses to other organs, including the lungs, liver, bone and bone marrow. It is characterized by the presence of Reed-Sternberg cells. Currently, there is no known cause of the disease, but the Epstein-Barr virus, HIV and familial history are known risk factors. The disease is slightly more prevalent in men than women, and the median age is 38. Approximately 151,000 cases of HL exist in the U.S., and an estimated 8,000 new cases of HL will be diagnosed this year in the U.S.

About Myelodysplastic Syndromes (MDS) and Acute Myelogenous Leukemia (AML)

Myelodysplastic syndromes are a serious and life-threatening group of diseases in which the bone marrow does not function normally, resulting in the production of malformed or immature blood cells. The disease begins when a defect occurs in the genetic material (chromosomes) of one of the stem cells in the bone marrow. That stem cell in turn produces cells that carry the defect. The defective cells eventually predominate in the bone marrow and overwhelm healthy blood cells. These defective cells are less able to produce functioning blood cells, which results in low blood cell counts (cytopenias) in the bloodstream.

Without enough healthy blood cells - red, white and platelets - people with MDS are at risk for a variety o f symptoms and complications including anemia, weakness, fatigue, infection and bleeding. Bone marrow failure results in death from bleeding and infection in the majority of patients, while transformation from MDS to acute myelogenous leukemia (AML) occurs in up to 40 percent of patients. The highest incidence of MDS is in patients over 60 years of age.

According to the Aplastic Anemia and MDS International Foundation, approximately 10,000-30,000 new cases of MDS are diagnosed each year in the United States, although it is difficult to accurately determine the incidence because MDS is not a disease for which the Centers for Disease Control and Prevention (CDC) mandates reporting of cases.

About MethylGene

MethylGene Inc. (TSX:MYG) is a publicly-traded biopharmaceutical company focused on the discovery, development and commercialization of novel therapeutics for cancer. The Company focuses on some of the most promising areas of oncology such as histone deacetylase (HDAC) and kinase inhibitors. The Company's lead product is MGCD0103, an oral isotype-selective HDAC inhibitor presently in multiple clinical trials for solid tumors and hematological malignancies, including Phase II monotherapy and Phase I/II combination trials with Vidaza and Gemzar(r). MGCD265 is an oral kinase inhibitor targeting the c-Met, Tie-2, Ron and VEGF receptor tyrosine kinases. In addition, MethylGene has several preclinical HDAC programs in non-oncology indications such as fungal infections (clinical candidate MGCD290 in combination with azoles to overcome resistance) and Huntington's disease. The company also has a beta-lactamase program to overcome antibiotic resistance. MethylGene's development and commercialization partners include Pharmion Corporation, Taiho Pharmaceutical,

Merck and EnVivo Pharmaceuticals. Please visit our website at www.methylgene.com.

About Pharmion

Pharmion is a biophar maceutical company focused on acquiring, developing and commercializing innovative products for the treatment of hematology and oncology patients in the U.S., Europe and additional international markets. Pharmion has a number of products on the market including the world's first approved epigenetic drug, Vidaza, a DNA demethylating agent. For additional information about Pharmion, please visit the company's website at www.pharmion.com.

MethylGene Inc.

Investor Relations Contacts:

Rhonda Chiger, Rx Communications Group, LLC

Phone: 917-322-2569

rchiger@rxir.com

Donald F. Corcoran

MethylGene Inc.

President & CEO

Phone: 514-337-3333 ext. 373

Pharmion Corporation

Breanna Burkart

Director, Investor Relations and Corporate Communications

Pharmion Corporation

Phone: +1 720.564.9144

Anna Sussman

Director, Investor Relations and Corporate Communications

Pharmion Corporation

Phone: +1 720.564.9143

Tara May

On-site Media Contact

Phone: +1 303.646.7832

Certain statements contained in this news release, other than statements of fact that are independently verifiable at the date hereof, may constitute forward-looking statements. Such statements, based as they are on the current expectations of management of MethylGene, inherently involve numerous risks and uncertainties, known and unknown, many of which are beyond MethylGene's control. These risks and uncertainties could cause future results, performance or achievements to differ significantly from the results, performance or achievements expressed or implied by such forward-looking statements. Such results, performance or achievements include, but are not limited to, the timing and effects of regulatory action; the continuation of collaborations; the results of clin ical trials; the timing of enrollment or completion of clinical trials; the success, efficacy or safety of MGCD0103, MGCD265 or MGCD290; the ability to scale up, formulate and manufacture sufficient GMP, clinical or commercialization quantities of MGCD0103, MGCD265 or MGCD290, and the relative success or the lack of success in developing and gaining regulatory approval and/or market acceptance for any compound or new product including MGCD0103, MGCD265 or MGCD290. Such risks include, but are not limited to, the impact of general economic conditions, economic conditions in the pharmaceutical industry, changes in the regulatory environment in the jurisdictions in which MethylGene does business, stock market volatility, fluctuations in costs, expectations with respect to our intellectual property position and our ability to protect our intellectual property and operate our business without infringing upon the intellectual property rights of others, changes in the competitive landscape including changes in the standard of care for the various indications in which MethylGene is involved, and changes to the competitive environment due to consolidation, as well as other risks, which you are urged to read, as described in MethylGene's Annual Information Form for the fiscal year ending December 31, 2006, under the heading 'risk factors,' the final prospectus filed on February 23, 2007, and all other documents filed by the Company that can be found at www.sedar.com. Consequently, actual future results may differ materially from the anticipated results expressed in the forward-looking statements. The reader should not place undue reliance on the forward-looking statements included in this presentation. These statements speak only as an update on the date they are made and MethylGene is under no obligation to revise such statements as a result of any event, circumstance or otherwise except in accordance with law.

Safe H arbor Statement under the Private Securities Litigation Reform Act of 1995: This release contains forward-looking statements, including summary statements relating to interim or preliminary results of clinical trials involving MGCD0103. Such statements are based on current expectations and involve a number of known and unknown risks and uncertainties that could cause the final results to differ significantly from the results summarized by such statements. Some of the clinical trials described in this release are being conducted by independent investigators and Pharmion does not control and cannot predict the final results of those trials. Top line or preliminary results may not be confirmed upon full analysis of the detailed results of a trial and additional information relating to the safety, efficacy or tolerability of MGCD0103 may be discovered upon further analysis of clinical trial data and upon review and analysis of data from other clinical trials. Additional risks and uncertainties relating to Pharmion and its business can be found in the "Risk Factors" section of Pharmion's Quarterly Report on Form 10-Q for the quarterly period ended March 31, 2007, its Annual Report on Form 10-K for the year ended December 31, 2006 and in Pharmion's other filings with the U.S. Securities and Exchange Commission. Forward-looking statements speak only as of the date on which they are made, and Pharmion undertakes no obligation to update publicly or revise any forward-looking statement, whether as a result of new information, future developments or otherwise. Pharmion also disclaims any duty to comment upon or correct information that may be contained in reports published by the investment community.

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Clinical Data Presented on Pilot Pharmacokinetic Study of Oral Azacitidine

Bioavailability Data from First Oral Demethylating Agent in Clinical Trials Presented at the American Society of Clinical Oncology 4 3rd Annual Meeting

CHICAGO, Ill., June 2, 2007 - Pharmion Corporation (NASDAQ: PHRM) today reported data from a pilot study that demonstrated the bioavailability of the Company's oral dosage formulation of Azacitidine. These data were presented at the 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO) in Chicago. (June 1-5, 2007). Pharmion's epigenetic anti-cancer products, which include Vidaza(r) (azacitidine for injection), MCGD0103 and oral Azacitidine, are being investigated in the treatment of hematologic malignancies and solid tumors and are the subject of poster and oral presentations at the Meeting.

An oral dosage formulation of Azacitidine would provide a more desirable and convenient route of administration for patients and clinical staff and eliminate injection-site reactions. In addition, it would enable the evaluation of a low-dose regimen that could maximize demethylation and gene re-expression, as well as the evaluation of long-term or maintenance therapy.

The study was designed to assess the safety, tolerability, and pharmacokinetics of escalating single doses of orally administered Azacitidine in patients with Myelodysplastic Syndromes (MDS), acute myeloid leukemia (AML) or other solid tumors. A total of four patients were enrolled and received study drug. One patient received a 60 mg dose and three patients received a single 80 mg dose. In each case, Azacitidine was well-tolerated and quantifiable in plasma. Following an 80mg dose the bioavailability of the oral formulation of Azacitidine was 18 percent relative to subcutaneous (SC) administered Vidaza. Having established that acceptable plasma concentrations of azacitidine can be achieved with single oral dosing, this pilot study has concluded. A multi-dose escalating study of oral azacitidine is now underway.

"Oral azacitidine represents an extremely exciting opportunity," said Dr. Guillermo Garcia-Manero, Associate Professor of Medicine and Chief, Section of Myelodysplastic Syndromes, Department of Leukemia, M.D. Anderson Cancer Center. "The potential for a chronic oral demethylating agent will not only apply to MDS but to many other tumor types as well. This is a very important step forward for epigenetic therapies."

Data Presented Saturday, June 2

Phase I/II study of a novel oral isotype-selective histone deacetylase (HDAC) inhibitor MGCD0103 in combination with azacitidine in patients (pts) with high-risk Myelodysplastic Syndrome (MDS) or Acute Myelogenous Leukemia (AML) - G. Garcia-Manero, MD, MD Anderson Cancer Center; Abstract #7062; June 2, 2007; 8:00-12:00 pm; McCormick Convention Center, S Hall A2

The combination of 5-azacytidine and valproic acid is safe and active in advanced solid tumors - A.O. Soriano, MD Anderson Cancer Center; Abstract #3547; June 2, 2007; 2:00-6:00pm; McCormick Place Convention Center, S102a

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Contact details

Breanna Burkart or Anna Sussman

Directors, Investor Relations and Corporate Communications

Pharmion Corporation

Tel: +1 720 564 9144 or +1 720 564 9143

Tara May

On-site media contact

Tel: +1 303 646 7832

About Vidaza

Vidaza was the first drug approved for the treatment of all five subtypes of myelodysplastic syndromes (MDS), including refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS) (if accompanied by neutropenia or thrombocytopenia or requiring transfusions), refractory anemia with excess blasts (RAEB), refractory anemia with excess blasts in transformation (RAEB-T), and chronic myelomonocytic leukemia(CMMoL).

Vidaza is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on abnormal hematopoietic cells in the bone marrow. The concentration of azacitidine required for maximum inhibition of DNA methylation in vitro does not cause major suppression of DNA synthesis. Hypomethylation m ay restore normal function to genes that are critical for differentiation and proliferation. The cytotoxic effects of azacitidine cause the death of rapidly dividing cells, including cancer cells that are no longer responsive to normal growth control mechanisms. Non-proliferating cells are relatively insensitive to Vidaza.

Important Safety Information

Vidaza is contraindicated in patients with a known hypersensitivity to azacitidine or mannitol and in patients with advanced malignant hepatic tumors. In clinical studies, the most commonly occurring adverse reactions were nausea (70.5%), anemia (69.5%), thrombocytopenia (65.5%), vomiting (54.1%), pyrexia (51.8%), leukopenia (48.2%), diarrhea (36.4%), fatigue (35.9%), injection site erythema (35.0%), constipation (33.6%), neutropenia (32.3%) and ecchymosis (30.5%). Other adverse reactions included dizziness (18.6%), chest pain (16.4%), febrile neutropenia(16.4%), myalgia (15.9%), injection site reaction (13.6%), aggravated fatigue (12.7%) and malaise (10.9%). Because treatment with Vidaza is associated with neutropenia and thrombocytopenia, complete blood counts should be performed as needed to monitor response and toxicity, but at a minimum, prior to each dosing cycle. Because azacitidine is potentially hepatotoxic in patients with severe pre-existing hepatic impairment, caution is needed in patients with liver disease. In addition, azacitidine and its metabolites are substantially excreted by the kidneys and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, it may be useful to monitor renal function. Vidaza may cause fetal harm. While receiving treatment with Vidaza, women of childbearing potential should avoid becoming pregnant, and men should avoid fathering a child. In addition, women treated with Vidaza should not nurse.

About MDS

The highest prevalence of MDS is i (Vidaza) in patients with Myelodysplastic Syndromes (MDS) - R. Lyons; Abstract #7083; June 2, 2007; 8am-12pm; McCormick Place Convention Center, S Hall A2)

Interim results from a Phase II, multi-center, open-label trial comparing three alternate dosing schedules of Azacitidine (AZA) in patients with MDS were presented in a poster session on Saturday, June 2. Patients were randomized to one of three regimens that were repeated every four weeks: AZA 5-2-2 (75 mg/m2/day x 5 days, two days off therapy, two additional days at same dose as the first five days); AZA 5-2-5 (50 mg/m2/day x 5 days, followed by 2 days off therapy and five additional days at the same dose as the first five days); and AZA 5 (75 mg/m2/day x 5 days).

Of 122 patients who had received two or more cycles of therapy at the time of evaluation, 61 percent experienced hematologic improvement (HI), defined as major or minor in at least one cell line. This reflects HI of 53, 70 and 60 percent in the AZA 5-2-2, AZA 5-2-5, and AZA 5 arms, respectively.

Across each of the three alternative dose regimens, 65 percent to 80 percent of patients who were red blood cell (RBC) transfusion dependent at baseline achieved transfusion independence. Comparable beneficial effects on transfusions were demonstrated in all patients and in low-risk patients for both RBCs and platelets.

To determine whether response/improvement can be maintained after six cycles, the study includes a 12 month maintenance period, in which patients are re-randomized to one of two arms: AZA 5 every four weeks or AZA 5 every six weeks. Ten patients have completed 18 treatment cycles.

These data indicate that the three alternative azacitidine dosing schedules have safety and efficacy profiles consistent with the FDA-approved regimen. Alternate dosing schedules may offer patients and clinicians a more convenient schedule by eliminating weekend treatments. Vidaza was the first demethylating agent to be approved by n patients over 60 years of age. According to the American Cancer Society and the Aplastic Anemia and MDS International Foundation, there are approximately 10,000-30,000 new cases of MDS in the United States each year. Survival ranges from six months to many years for the different subtypes of MDS.

About Epigenetics

DNA methylation and histone deacetylation are two of the more studied epigenetic regulators of gene expression. Epigenetics refers to changes in the regulation of gene expression. Epigenetic changes can silence gene expression and, unlike DNA mutations, may be reversed by targeting the enzymes involved. The silencing of key cell cycle control genes and tumor suppressor genes through these two mechanisms of epigenetic regulation have been demonstrated in vitro and in vivo in hematological malignancies and in solid tumors. Vidaza has been shown to reverse the effects of DNA hypermethylation with subsequent gene re-expression and likewise MGCD0103 has been shown, in vivo, to reverse the effects of inappropriate deacetylation resulting in gene expression reactivation. The epigenetic approach to cancer therapy is that rather than using molecules that kill both normal and tumor cells, the silenced genes are reactivated through targeted epigenetic therapy, re-establishing the cancer cell's natural mechanisms to control abnormal growth.

About Pharmion

Pharmion is a biopharmaceutical company focused on acquiring, developing and commercializing innovative products for the treatment of hematology and oncology patients in the U.S., Europe and additional international markets. Pharmion has a number of products on the market including the world's first approved epigenetic drug, Vidaza(r), a DNA demethylating agent. For additional information about Pharmion, please visit the company's website at www.pharmion.com <http://www.pharmion.c om/> .

Safe Harbor Statement under the Private Securities Litigation Reform Act of 1995:

This release contains forward-looking statements, including summary statements relating to interim or preliminary results of clinical trials involving oral azacitidine. Such statements are based on current expectations and involve a number of known and unknown risks and uncertainties that could cause the final results to differ significantly from the results summarized by such statements. Some of the clinical trials described in this release are being conducted by independent investigators and Pharmion does not control and cannot predict the final results of those trials. Top line or preliminary results may not be confirmed upon full analysis of the detailed results of a trial and additional information relating to the safety, efficacy or tolerability of oral azacitidine may be discovered upon further analysis of clinical trial data and upon review and analysis of data from other clinical trials. Additional risks and uncertainties relating to Pharmion and its business can be found in the "Risk Factors" section of Pharmion's Quarterly Report on Form 10-Q for the quarterly period ended March 31, 2007, its Annual Report on Form 10-K for the year ended December 31, 2006 and in Pharmion's other filings with the U.S. Securities and Exchange Commission. Forward-looking statements speak only as of the date on which they are made, and Pharmion undertakes no obligation to update publicly or revise any forward-looking statement, whether as a result of new information, future developments or otherwise. Pharmion also disclaims any duty to comment upon or correct information that may be contained in reports published by the investment community.

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Exelixis Reports Comprehensive XL880 Phase I Data At ASCO

-Results support ongoing Phase II clinical development program-

CHICAGO, June 2 /PRNewswire-Fi rstCall/ -- Exelixis, Inc. (Nasdaq: EXEL) reported data from the Phase I clinical trial program for XL880, a novel small molecule compound that simultaneously inhibits MET and VEGFR2, targets implicated in tumor growth, tumor cell migration, and angiogenesis. Patricia M. LoRusso, D.O., Director of the Phase I Clinical Trials Program at the Barbara Ann Karmanos Cancer Institute, Professor of Hematology and Oncology at Wayne State University, and a lead investigator in the trial, presented the data in the Developmental Therapeutics: Molecular Therapeutics oral abstract session (Abstract #3526) at the 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO).

The data presented were taken from two Phase I studies of XL880 in patients with advanced solid tumors. One study evaluated an intermittent, weight-based dosing regimen and the other evaluated fixed daily dosing. Both studies included pharmacokinetic, pharmacodynamic, and tumor response analyses.

Five partial responses (>30% tumor regression by RECIST) were observed, including three in papillary renal cell cancer, one in medullary thyroid cancer, and one in hurthle cell thyroid cancer. Tumor shrinkage of less than 30% or prolonged stable disease of greater than 3 months was observed in an additional 20 patients. Additionally, in a best response evaluation as determined by RECIST criteria, investigators reported that 39 of 45 patients in the combined phase 1 studies had either tumor regression or stable disease.

"We consider the number of patients with responses or disease stabilization in these studies to be quite striking, particularly in light of these patients' advanced disease," said Dr. LoRusso. "We believe XL880 has significant potential as a novel cancer therapy, and the ongoing Phase II trials should provide important insight into the late stage development plans for the compound."

Histological analyses of tumor samples from four patients showed decreases in the ph osphorylation of MET following administration of XL880. These decreases resulted in predicted downstream effects, including reduction of phosphorylated AKT levels and markedly increased tumor cell death. These effects were not observed in control samples of normal tissue obtained from the same patients. Pharmacokinetic analyses showed that peak and average concentrations over 28 days were higher with intermittent compared with daily dosing of XL880, reflecting the higher dose administered with the intermittent schedule, and the compound's long half life.

The data indicate that XL880 was generally well tolerated, and that the reported side effects were treatable and reversible. Dose limiting toxicities included hypertension, dehydration, hand-foot syndrome, tumor hemorrhage, and elevation of liver enzymes and lipase. Most of the common reported side effects are consistent with previously identified effects associated with inhibition of VEGF signaling, such as hypertension and proteinuria. Elevations in liver function tests also were observed and considered possibly related to XL880.

"We believe these results clearly demonstrate that XL880 simultaneously inhibits both MET and VEGFR2 in this clinical setting," said Michael M. Morrissey, Ph.D., president of research and development at Exelixis. "Inhibition of both MET and VEGFR2 abrogates two major mechanisms tumors use to survive in hypoxic conditions. The clinical data with XL880 suggest that dual MET/VEGFR2 inhibition has the potential to translate into meaningful anti-tumor activity in patients with advanced cancer."

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About XL880

XL880 has attractive pharmaceutical properties, with high solubility and oral bioavailability. In preclinical studies, XL880 inhibited its targets with nanomolar potency, and retained potent activity against mutationally activated forms of MET found in hereditary papillary renal cell carcinomas. The compound also demonstrated dose-dependent tu mor growth inhibition in models of breast cancer, colorectal cancer, non-small cell lung cancer, and glioblastoma, and has been shown to cause substantial tumor regression in all models tested. Significantly, a single dose of XL880 completely inhibited tumor growth for 21 days in a glioblastoma model.

About Exelixis

Exelixis, Inc. is a development-stage biotechnology company dedicated to the discovery and development of novel small molecule therapeutics for the treatment of cancer and other serious diseases. The company is leveraging its fully integrated drug discovery platform to fuel the growth of its development pipeline, which is primarily focused on cancer. Currently, Exelixis' broad product pipeline includes investigational compounds in Phase II and Phase I clinical development for cancer and renal disease. Exelixis has established strategic corporate alliances with major pharmaceutical and biotechnology companies, including GlaxoSmithKline, Bristol-Myers Squibb Company, Genentech, Wyeth Pharmaceuticals and Sankyo. For more information, please visit the company's web site at www.exelixis.com.

This press release contains forward-looking statements, including without limitation statements related to the potential efficacy of XL880. Words such as "suggest," "believes," "indicates," "should," and similar expressions are intended to identify forward-looking statements. These forward-looking statements are based upon Exelixis' current expectations. Forward-looking statements involve risks and uncertainties. Exelixis' actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, which include, without limitation, the potential failure of XL880 to demonstrate safety and efficacy in clinical testing. These and other risk factors are discussed under "Risk Factors" and elsewhere in Exelixis' quarterly report on Form 10-Q for the fiscal quarter ended March 30, 2007 and other filings with the Securities and Exchange Commission. Exelixis expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in the company's expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based.

SOURCE Exelixis, Inc.

Investor Contact: Charles Butler, Director, Corporate Communications,

+1-650-837-7277, cbutler@exelixis.com, or

Media Contact: Hal Mackins, Corporate Communications,

+1-650-837-7012, hmackins@exelixis.com, both of Exelixis, Inc.

Web site: http://www.exelixis.com <http://www.exelixis.com/>

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Exelixis Reports Integrated Data From Phase II Clinical Trials of XL999 at ASCO

CHICAGO, June 3, 2007 /PRNewswire-FirstCall via COMTEX News Network/ -- Exelixis, Inc. (Nasdaq: EXEL) reported integrated data from six Phase II clinical trials of XL999 in patients with non-small cell lung cancer (NSCLC), renal cell carcinoma, metastatic colorectal cancer, recurrent ovarian cancer, acute myelogenous leukemia (AML), and multiple myeloma. Results show preliminary anti-tumor activity in patients with NSCLC and AML, as well as a cardiovascular adverse event profile consistent with previously reported data. The data were presented in a poster session on Sunday, June 3, 2007 (Abstract #3591) at the 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO).

The primary objectives of each trial were to determine the response rate and to further evaluate the safety and tolerabilit y of XL999. Secondary objectives were to assess progression-free survival, duration of response, and overall survival with XL999. Patients in the studies received a once-weekly, 4-hour intravenous infusion of XL999 dosed at 2.4 mg/kg.

"We believe this integrated report provides a clear basis for the further development of XL999 with an appropriate risk-benefit profile," said Gisela M. Schwab, MD, senior vice president and chief medical officer at Exelixis. "On the basis of these data, further clinical evaluation of XL999 is planned in patients with stage IIIB-IV NSCLC in a Phase I dose-escalation study."

Integrated results from 79 patients who participated in the Phase II trials show preliminary evidence of XL999 activity in patients with NSCLC or AML. Of nine patients in the trial with NSCLC, two had partial responses (6 months and 11+ months), and three had stable disease for at least three months. Fourteen AML patients participated in the trial, of which ten had circulating myeloblasts. Eight of these ten patients experienced at least a 50% reduction in circulating myeloblasts following administration of XL999, one of whom achieved a partial response. Three of the 14 AML patients were found to have activating mutations in FLT3, including the patient who achieved a partial response. All three of these patients experienced a greater than 98% reduction in circulating myeloblasts.

With respect to the safety of XL999, serious cardiac adverse events occurred in 11 of the 79 patients (14%). These events were associated with the dose rate of XL999 and generally were associated with the first dose. Cardiac adverse events varied in severity, ranging from asymptomatic ECG changes to cardiopulmonary failure, and usually improved with discontinuation of XL999. Nine other non-cardiac serious adverse events associated with XL999 were reported: diarrhea (1), asthenia (1), pyrexia (2), hypersensitivity (2), vena cava thrombosis (1), dehydration (1), and pulmo nary hemorrhage (1).

Clinical development of XL999 was re-initiated in April 2007. This clinical trial will evaluate XL999 in patients with NSCLC who have failed at least one previous therapy. The trial will have a dose-escalation format starting at 0.4 mg/kg dosed weekly, while monitoring patients for potential cardiovascular events. Results from this Phase I clinical trial could provide Exelixis with the opportunity to move directly into a late stage clinical trial if XL999 demonstrates anti-tumor activity with an acceptable side-effect profile in this well-defined NSCLC patient population. Exelixis expects to begin enrolling patients in this trial during the summer of 2007.

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About XL999

XL999 is a potent inhibitor of key receptor tyrosine kinases implicated in the development and maintenance of tumor vasculature, and in the proliferation of some tumor cells. It inhibits FGFR1, FGFR3, RET, VEGFR2, and PDGFR. The compound is also a potent inhibitor of FLT3, an important driver of leukemia cell proliferation in some patients with acute myelogenous leukemia (AML). XL999 exhibited potent activity in preclinical target-specific pharmacodynamic models, as well as efficacy models for solid tumors and for FLT3-driven leukemia.

About Exelixis

Exelixis, Inc. is a development-stage biotechnology company dedicated to the discovery and development of novel small molecule therapeutics for the treatment of cancer and other serious diseases. The company is leveraging its fully integrated drug discovery platform to fuel the growth of its development pipeline, which is primarily focused on cancer. Currently, Exelixis' broad product pipeline includes investigational compounds in Phase II and Phase I clinical development for cancer and renal disease. Exelixis has established strategic corporate alliances with major pharmaceutical and biotechnology companies, including GlaxoSmithKline, Bristol-Myers Squibb Company, Genentech, Wyet h Pharmaceuticals and Sankyo. For more information, please visit the company's web site at www.exelixis.com.

This press release contains forward-looking statements, including without limitation statements related to the safety and potential efficacy of XL999 Words such as "believes," "may," "expects," "plan," "will" and similar expressions are intended to identify forward-looking statements. These forward-looking statements are based upon Exelixis' current expectations. Forward-looking statements involve risks and uncertainties. Exelixis' actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, which include, without limitation, risks related to the lengthy, costly and uncertain process of clinical testing of XL999 and the potential failure to demonstrate safety and efficacy and the therapeutic potential of XL999. These and other risk factors are discussed under "Risk Factors" and elsewhere in Exelixis' quarterly report on Form 10-Q for the fiscal quarter ended March 30, 2007 and other filings with the Securities and Exchange Commission. Exelixis expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward- looking statements contained herein to reflect any change in the company's expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based.

SOURCE Exelixis, Inc.

Investor Contact: Charles Butler, Director, Corporate Communications,

+1-650-837-7277, cbutler@exelixis.com, or Media Contact: Hal Mackins,

+Corporate

Communications, +1-650-837-7012, hmackins@exelixis.com, both of Exelixis, Inc.

http://www.exelixis.com <http://www.exelixis.com/>

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the FDA and the first approved treatment for all five subtypes of MDS.

The combination of azacitidine (Vidaza) and valproic acid is safe and active in advanced solid tumors - A.O. Soriano; Abstract #3547; June 2, 2007; 2-6pm; McCormick Place Convention Center, S102a

Results were reported this afternoon from a Phase I study of Azacitidine, a DNA hypomethylating agent, in combination with valproic acid, an HDAC inhibitor, in patients with advanced solid tumors. The study, which included patients with advanced forms of 10 different solid tumors, evaluated the safety and activity of the two compounds in combination.

Of 55 evaluable patients, 14 patients, or 25 percent, were observed to experience stable disease in a variety of advanced solid tumors. The duration of the patients' stable disease was four to 12 months, with a median of six months.

These data show that the combination of the two compounds was safe and active in patients with advanced solid tumors The data also indicated that the maximum tolerated dose of azacitidine when used in the combination was 75 mg/m2. Significant global DNA hypomethylation and histone acetylation were demonstrated.

Data Presented Saturday, June 2

Phase I/II study of a novel oral isotype-selective histone deacetylase (HDAC) inhibitor MGCD0103 in combination with Azacitidine in patients (pts) with high-risk Myelodysplastic Syndrome (MDS) or Acute Myelogenous Leukemia (AML) - G. Garcia-Manero, MD, MD Anderson Cancer Center; Abstract #7062; June 2, 2007; 8:00-12:00 pm; McCormick Convention Center, S Hall A2

The combination of 5-azacytidine and valproic acid is safe and active in advanced solid tumors - A.O. Soriano, MD Anderson Cancer Center; Abstract #3547; June 2, 2007; 2:00-6:00pm; McCormick Place Convention Center, S102a

Tolerability and hematologic improvement assessed using three alternative dosing schedules of azacitidine (Vidaza) in patients with MDS - R. Lyons, US Oncology; Abstract #7083; June 2, 2007; 8:00am-12:00pm; McCormick Place Convention Center, S Hall A2

An oral dosage formulation of azacitidine: A pilot pharmacokinetic study - R. Ward, Pharmion; Abstract #7084; June 2, 2007; 8:00am-12:00pm; McCormick Place Convention Center, S Hall A2

Response to azacitidine in patients with myelodysplastic syndrome with marrow fibrosis - R. Juvvadi, Western Penn, Pennsylvania; Abstract #7089; June 2, 2007; 8:00am-12:00pm; McCormick Place Convention Center, S Hall A2

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Contact details

Breanna Burkart or Anna Sussman

Directors, Investor Relations and Corporate Communications

Pharmion Corporation

Tel: +1 720 564 9144 or +1 720 564 9143

Tara May

On-site media contact

Tel: +1 303 646 7832

About Vidaza

On May 19, 2004, Vidaza became the first drug approved by the FDA for the treatment of patients with Myelodysplastic Syndromes (MDS). The FDA approved Vidaza, the first in a new class of drugs called demethylation agents, for treatment of all five MDS subtypes, which include both low-risk and high-risk patients. These subtypes include: refractory anemia (RA) or refractory anemia with ringed sideroblasts (RARS) if accompanied by neutropenia or thrombocytopenia or requiring transfusions; refractory anemia with excess blasts (RAEB), refractory anemia with excess blasts in transformation (RAEB-T), and chronic myelomonocytic leukemia (CMMoL).

Vidaza is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on abnormal hematopoietic cells in the bone marrow. The concentration of azacitidine required for maximum inhibition of DNA methylation in vitro does not cause major suppression of DNA synthesis. Hypomethylation may restore normal function to genes that are critical for differentiation and proliferation. The cytotoxic effects of azacitidine cause the death of rapidly dividing cells, including can cer cells that are no longer responsive to normal growth control mechanisms. Non-proliferating cells are relatively insensitive to Vidaza.

About Epigenetics

Azacitidine is the first of a new class of anti-cancer compounds called epigenetic therapies. DNA methylation and histone deacetylation are two of the more studied epigenetic regulators of gene expression. Epigenetics refers to changes in the regulation of gene expression. Epigenetic changes can silence gene expression and, unlike DNA mutations, may be reversed by targeting the enzymes involved. The silencing of key cell cycle control genes and tumor suppressor genes through these two mechanisms of epigenetic regulation has been demonstrated in vitro and in vivo in hematological malignancies and in solid tumors. These key growth control genes can be re-expressed in cancer cells when DNA hypermethylation is reversed by Vidaza and/or inappropriate histone deacetylation is inhibited by MGCD0103. The epigenetic approach to cancer therapy is that rather than using molecules that kill both normal and tumor cells, the silenced genes are reactivated through targeted epigenetic therapy, re-establishing the cancer cell's natural mechanisms to control abnormal growth.

Important Safety Information

Vidaza is contraindicated in patients with a known hypersensitivity to azacitidine or mannitol and in patients with advanced malignant hepatic tumors.

In clinical studies, the most commonly occurring adverse reactions by SC route were nausea (70.5%), anemia (69.5%), thrombocytopenia (65.5%), vomiting (54.1%), pyrexia (51.8%), leukopenia (48.2%), diarrhea (36.4%), fatigue (35.9%), injection site erythema (35.0%), constipation (33.6%), neutropenia (32.3%) and ecchymosis (30.5%). Other adverse reactions included dizziness (18.6%), chest pain (16.4%), febrile neutropenia (16.4%), myalgia (15.9%), injection site reaction (13.6%), aggravated fatigue (12.7%) and malaise (10.9%). The most common adverse reactions by IV route also included petechiae (45.8%), rigors (35.4%), weakness (35.4%) and hypokalemia (31.3%).

Because treatment with Vidaza is associated with neutropenia and thrombocytopenia, complete blood counts should be performed as needed to monitor response and toxicity, but at a minimum, prior to each dosing cycle.

Because azacitidine is potentially hepatotoxic in patients with severe pre-existing hepatic impairment, caution is needed in patients with liver disease. In addition, azacitidine and its metabolites are substantially excreted by the kidneys and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, it may be useful to monitor renal function.

Vidaza may cause fetal harm. While receiving treatment with Vidaza, women of childbearing potential should avoid becoming pregnant, and men should avoid fathering a child. In addition, women treated with Vidaza should not nurse.

About Pharmion

Pharmion is a biopharmaceutical company focused on acquiring, developing and commercializing innovative products for the treatment of hematology and oncology patients in the U.S., Europe and additional international markets. Pharmion has a number of products on the market including the world's first approved epigenetic drug, Vidaza(r), a DNA demethylating agent. For additional information about Pharmion, please visit the company's website at www.pharmion.com <http://www.pharmion.com/> .

Safe Harbor Statement under the Private Securities Litigation Reform Act of 1995:

This release and the presentations referred to in this release contain forward-looking statements, including summary statements relating to interim or preliminary results of clinical trials involving Vidaza. Such statements are ba sed on current expectations and involve a number of known and unknown risks and uncertainties that could cause the final results to differ significantly from the results summarized by such statements. Some of the clinical trials described in this release are being conducted by independent investigators and Pharmion does not control and cannot predict the final results of those trials. Top line or preliminary results may not be confirmed upon full analysis of the detailed results of a trial and additional information relating to the safety, efficacy or tolerability of Vidaza may be discovered upon further analysis of clinical trial data and upon review and analysis of data from other clinical trials. Additional risks and uncertainties relating to Pharmion and its business can be found in the "Risk Factors" section of Pharmion's Quarterly Report on Form 10-Q for the quarterly period ended March 31, 2007, its Annual Report on Form 10-K for the year ended December 31, 2006 and in Pharmion's other filings with the U.S. Securities and Exchange Commission. Forward-looking statements speak only as of the date on which they are made, and Pharmion undertakes no obligation to update publicly or revise any forward-looking statement, whether as a result of new information, future developments or otherwise. Pharmion also disclaims any duty to comment upon or correct information that may be contained in reports published by the investment community.

# # #

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PHARMION AND METHYLGENE REPORT PRELIMINARY DATA FOR MGCD0103 AT THE 43rd AMERICAN SOCIETY OF CLINICAL ONCOLOGY (ASCO) ANNUAL MEETING

HDAC INHIBITOR MGCD0103 DEMONSTRATES substantial RESPONSE RATE IN TWO CLINICAL TRIALS

40% Response Rate and 45% Disease Control Rate in Single-Agent Phase II Trial in Refractory or Relapsed Hodgkin's Lymphoma Patients

30% Response Rate (37% at Relevant Active Doses) in Phase I/II Combination Trial with Vidaza(r) in MD S and AML Patients

CHICAGO, Ill. June 2, 2007 - Pharmion Corporation (NASDAQ:PHRM) and MethylGene Inc. (TSX:MYG) today announced preliminary Phase II and Phase I/II data for their lead oncology product candidate, MGCD0103, a novel, isotype-selective histone deacetylase (HDAC) inhibitor which showed significant anti-tumor activity in patients with Hodgkin's lymphoma, Myelodysplastic Syndromes and acute myelogenous leukemia. The data were presented Saturday at the 43rd American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago.

Hodgkin's Lymphoma (Trial 010)

Data presented show an objective complete and partial response rate of 40 percent and a disease control rate of 45 percent in a population of patients that had relapsed disease or were refractory (unresponsive) to all previous treatments, including, in many cases, bone marrow transplantation. Overall, 75 percent of patients experienced a reduction in tumor size, with 60 percent experiencing a tumor reduction of greater than 30 percent.

"It is striking that single-agent therapy with MGCD0103 achieved such impressive objective clinical responses in this population," said Anas Younes, M.D., principal investigator and Professor of Medicine and Director, Clinical Investigation and Translational Research in the Department of Lymphoma/Myeloma, M.D. Anderson Cancer Center. "No approved therapies exist for patients suffering from Hodgkin's lymphoma that has progressed following transplantation. With a novel mechanism of action and an oral route of administration, MGCD0103 would be a welcome and desirable addition to the Hodgkin's lymphoma armamentarium."

The data were presented as part of a clinical symposium titled, "Breaking the Silence of the Genome: HDAC Inhibitors," which focused on the progress and potential of this emerging therapeutic category. The HDACs are enzymes that mediate histone deacetylation, an epigenetic form of gene regulation that may silence tumor suppres sor genes, thereby promoting tumor growth. MGCD0103 is an orally-administered, selective HDAC inhibitor, which targets specific class I HDAC isotypes. Preclinical data suggest that these HDAC isotypes are important in cancer biology and, consequently, such selective HDAC inhibitors may have increased efficacy and reduced toxicity compared to non-selective inhibitors.

Myelodysplastic Syndrome (MDS) and Acute Myelogenous Leukemia (AML) (Trial 005)

Data presented in a poster session by Guillermo Garcia-Manero, M.D., principal investigator, Associate Professor of Medicine and Chief, Section of Myelodysplastic Syndromes, Department of Leukemia, M.D. Anderson Cancer Centre, demonstrated that combination treatment with MGCD0103 and Vidaza(r) (azacitidine for injection) resulted in a 30 percent response rate for all patients, and a 37 percent response rate in the active dose ranges previously reported. Of the 37 patients in this trial, eleven patients (two MDS patients and nine AML patients) experienced objective clinical responses. In addition, the combination therapy showed good pharmacodynamic properties and acceptable safety in these patients.

"MGCD0103 and Vidaza are two epigenetic agents that have demonstrated single-agent activity in AML and MDS," said Dr. Garcia-Manero. "In this study we found that these agents can be given together, and that the resulting clinical activity is better than expected from each agent alone."

"We are very encouraged by the single-agent activity to date in our Hodgkin's lymphoma trial. These patients have progressive disease after receiving multiple prior therapies and there are currently no approved alternative treatments available to them," said Donald F. Corcoran, President and Chief Executive Officer of MethylGene. "In addition, the responses in our Vidaza-MGCD0103 combination trial are consistent with our earlier data. The data from these two ongoing trials have given us potential direction for registratio
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