Pharmion and MethylGene Present Favorable Clinical Data From Combination MGCD0103/Vidaza(R) Study in Myelodysplastic Syndromes and Acute Myelogenous Leukemia at The 49th American Society of Hematology (ASH) Meeting

* Recommended Phase II Dose of MGCD0103 Determined as 90 mg

ATLANTA, December 10, 2007 /PRNewswire-FirstCall/ -- Pharmion Corporation and MethylGene Inc today announced maturing data from the Phase 1/2 study investigating the combined use of MGCD0103, a novel, isotype-selective histone deacetylase (HDAC) inhibitor, and Vidaza(R) (azacitidine for injection) in patients with myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML). A 53 percent response rate (n=19) was demonstrated at the 90 mg dose with a median time to response of less than two months. The overall results indicate a 36 percent response rate for patients evaluated at all doses (n=52 evaluable patients) in this Phase 1/2 study. The data were presented in an oral presentation today at the 49th Annual Meeting and Exposition of the American Society of Hematology (ASH) in Atlanta.

"This study demonstrates the progress Pharmion has made in advancing the clinical development of these therapies in treating MDS and AML, and reinforces Pharmion's standing as a leader in epigenetic therapy," said Patrick J. Mahaffy, president and chief executive officer of Pharmion. "Together, Vidaza and MGCD0103 showcase Pharmion's highly complementary clinical hematology and oncology portfolio."

"This study and data from our other clinical trials continue to demonstrate MGCD0103's potential utility when used in combination or as a single-agent," said Donald F. Corcoran, President and Chief Executive Officer of MethylGene. "The results of this study provide the basis for our planned three-arm randomized study of MGCD0103 and Vidaza in AML and MDS patients."

The study entitled, "Phase I/II study of MGCD0103, an oral isotype-selective histone deacetylase (HDAC) Inhibitor, in combination with 5-azacitidine in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML)", Abstract #444 (Trial 005) was delivered as an oral presentation 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 Center.

Patients with MDS, relapsed/refractory AML, or untreated patients with AML were given Vidaza at its approved dose/schedule (75 mg/m2 SC daily for the first 7 days of a 28 day cycle). MGCD0103 was added orally three-times a week starting on the fifth day of Vidaza administration.

Of the 52 evaluable patients treated at all dose levels in the study (43 patients with AML and 9 with MDS), 36 percent (19 patients) demonstrated objective responses to the combined treatment (eight complete responses [CR], ten complete responses with incomplete peripheral count recovery [CRi], and one partial response [PR]). Among the 19 patients receiving MGCD0103 at a dose of 90 mg, 10 (53 percent) achieved a response. Of the 52 evaluable patients, 71 percent had received prior therapy. Of particular note, in an overall survival analysis, patients with a response had a 66 percent reduction in the risk of death when compared to non-responders.

The most common grade 3 and 4 non-hematological toxicities in the study were fatigue and gastrointestinal in nature (e.g., nausea, vomiting, anorexia, diarrhea, dehydration). The recommended phase 2 dose for MGCD0103 was determined to be 90 mg.

Vidaza did not affect MGCD0103 pharmacokinetics, nor did co-administration of MGCD0103 impact the pharmacokinetics of Vidaza. A majority of patients exhibited a substantial reduction in PBMC HDAC activity during treatment with the combination.

In summary, these results appear to support and form the basis of testing the combination therapy of MGCD0103 and Vidaza in a larger randomized three-arm study which is currently being planned by the partners.

About MGCD0103

MGCD0103 is an orally-administered, isotype-selective HDAC inhibitor. The compound is currently in three Phase I/II clinical trials, in combination with Vidaza(R) for hematological malignances and with Gemzar(R) and Taxotere(R) in solid tumors; and in four Phase II monotherapy clinical trials in hematological malignancies.

About Vidaza

In May 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. 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 Vidaza 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 Vidaza 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. Vidaza was approved for IV administration in January 2007.

About Epigenetic Therapy

DNA methylation and histone deacetylation are the two most studied epigenetic regulators of gene expression. Vidaza reverses the effects of DNA hypermethylation with subsequent tumor suppressor gene re-expression. MGCD0103 exerts its epigenetic effects by acting as an oral isotype-selective HDAC inhibitor. Together, the two act synergistically to induce suppressor gene re-expression and favorably influence the clinical course of cancer. Pharmion strongly believes that by targeting two separate epigenetic pathways simultaneously, the combination of drugs targeting DNA methylation and histone deacetylation can either increase the susceptibility of cancer cells to standard chemotherapy or act as a potent therapeutic regimen in its own right.

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 of 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.

Important Vidaza Safety Information

Vidaza is contraindicated in patients with a known hypersensitivity to Vidaza 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 Vidaza is potentially hepatotoxic in patients with severe pre- existing hepatic impairment, caution is needed in patients with liver disease. In addition, Vidaza 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 MethylGene

MethylGene Inc. is a publicly-traded biopharmaceutical company focused on the discovery, development and commercialization of novel therapeutics for cancer. The Company's lead product, MGCD0103, is an oral isotype-selective HDAC inhibitor presently in multiple clinical trials for solid tumors and hematological malignancies, including Phase 2 monotherapy and Phase 1/2 combination trials with Vidaza(R), Gemzar(R) and Taxotere(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 programs: MGCD290, an HDAC inhibitor in combination with azoles for fungal infections; an HDAC program for Huntington's disease; and a sirtuins program for cancer. MethylGene's development and commercialization partners include Pharmion Corporation, Taiho Pharmaceutical and EnVivo Pharmaceuticals. Please visit our website at http://www.methylgene.com.

About Pharmion

Pharmion is a leading global oncology company uniquely 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 http://www.pharmion.com.

Safe Harbor Statement under the Private Securities Litigation Reform Act of 1995: This release contains forward-looking statements, including summary statements relating to the interim or preliminary results of clinical trials involving Vidaza and 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. Preliminary results may not be confirmed upon final analysis of the detailed results of a trial and additional information relating to the safety, efficacy or tolerability of Vidaza and MGCD0103 may be discovered upon further analysis of clinical trial data and upon review and analysis of additional clinical trial data from this or 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 September 30, 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.

CONTACT: Breanna Burkart, Director, Investor Relations and CorporateCommunications, +1-720-564-9144, , or Anna Sussman,Director, Investor Relations and Corporate Communications, +1-720-564-9143,, both of Pharmion Corporation; or Rhonda Chiger of RxCommunications Group, LLC, +1-917-322-2569, , forMethylGene Inc.; or Donald F. Corcoran, President & CEO of MethylGene Inc.,+1-514-337-3333, ext. 373; or PHARMION ON-SITE MEDIA CONTACTS, Hal Mackinsof Ogilvy Public Relations, US, +1-415-994-0040, or Joanne Wunder, OgilvyPublic Relations, EU, +44-7801-082-574, for Pharmion Corporation bburkart@pharmion.com asussman@pharmion.com rchiger@rxir.com

Web site: http://www.pharmion.com/http://www.methylgene.com/

Ticker Symbol: (NASDAQ-NMS:PHRM),(Toronto:MYG.)

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Posted: December 2007

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