MAXIM PHARMACEUTICALS PRESENTS PRECLINICAL RESULTS FOR ITS NOVEL VASCULAR TARGETING AGENT MX116407

MAXIM PHARMACEUTICALS PRESENTS PRECLINICAL RESULTS FOR ITS NOVEL VASCULAR TARGETING AGENT MX116407 Results for MX116407 and MX90745 presented at American Association for Cancer Research Annual Meeting San Diego, California, March 30, 2004 - Maxim Pharmaceuticals (Nasdaq NM: MAXM, SSE: MAXM) today announced research results demonstrating the anti-cancer activity of the Company's MX116407 compounds at the 2004 American Association of Cancer Research (AACR) meeting in Orlando, Florida. Maxim scientists presented key results demonstrating that treatment with MX116407 as a single agent produced tumor regression in lung cancer animal models. MX116407 also produced a statistically significant enhancement of anti-tumor activity when combined with existing cytotoxics that was superior to the activity of other vascular targeting agents currently in clinical development under the auspices of other companies. MX116407 has been shown to induce apoptosis in cancer cells and in several animal efficacy xenograph models, including models of breast cancer, lung cancer and colorectal cancer. MX116407 is being prepared for studies designed to support the initiation of human clinical trials. The MX116407 preclinical results were reported in two presentations at the AACR meeting. Shailaja Kasibhatla, Ph.D., Maxim's Director, Cell Biology, reported the results of preclinical testing of MX116407 in a presentation titled "Discovery of a Novel Substituted Chromene Series as Apoptosis Inducers with Anti-Mitotic and Anti-Vasculature Activities." Sui Xiong Cai, Ph.D., Maxim's Senior Director, Chemistry, described the initial discovery and development of the compound series that led to the development of MX116407 in a presentation titled "Discovery and Structure-Activity Relationships of 4-Aryl-4H-Chromemes as a New Series of Apoptosis Inducers Using a Cell- and Caspase-Based High Throughput Screening Assay." MX116407 is the lead compound of Maxim's MX2105 series, which have been shown to induce apoptosis in cancer cells in preclinical testing. Dr. Kasibhatla reported that the MX2105 series of compounds have potent cytotoxic activity against proliferating cells and disrupt newly formed capillary tubes at low nanomolar concentrations, indicating that these compounds can potentially combat cancer through vascular targeting activity. Dr. Kasibhatla reported that MX116407 demonstrated potent efficacy in the MX-1 human breast cancer xenograph model in mice, producing a 90% inhibition of tumor growth compared to a 62% inhibition for ZD6126, another vascular targeting agent currently in clinical development. As a single agent in the Calu-6 human lung cancer xenograph model, MX116407 demonstrated statistically significant anti-tumor activity and produced tumor regression. In the same lung cancer model, the combination of MX116407 and the cytotoxic agent cisplatin demonstrated statistically significant anti-tumor activity and produced tumor regression and a cure rate of 40% compared to a cure rate of zero for the combination of cisplatin and Combretastatin-P (CA4-P), another vascular targeting agent currently in clinical development by another company. Other apoptosis inducer compounds discovered by Maxim were also the subjects of presentations at the AACR conference. Dr. Ben Tseng, Ph.D., Maxim's Senior Director, Research, reported the results of testing associated with the MX90745 series of compounds in a presentation titled "MX90745, a New Family of Apoptosis-Inducing Molecules with Potent In- Vivo Anti-Cancer Activities." The MX90745 series of apoptosis inducer compounds was licensed by Maxim to Myriad Genetics, Inc. last year. Under the license agreement Maxim is providing research services to Myriad to assist with the development of the MX90745 family. The antitumor activity of the lead compound from this series in breast, colon, pancreatic, ovarian and mouse melanoma tumor xenografts in athymic nude mice was also reported in a presentation by researchers from Myriad. Lastly, a compound discovered under Maxim's collaboration with Celera Genomics was the subject of two poster presentations by Celera's scientists at the AACR conference. "We are extremely pleased to have such a presence this year at AACR. These multiple presentations highlight the advancing development by our research group on several potential new anticancer agents identified through our highly productive discovery research program," says Kurt R. Gehlsen, Senior Vice President and Chief Scientific Officer. "Moreover, our licensing partners have clearly made significant progress with two of the compounds and we expect to see these investigational product candidates move into the clinic." Maxim Overview Maxim Pharmaceuticals is a global biopharmaceutical company with a diverse pipeline of therapeutic candidates for life-threatening cancers and liver diseases. Maxim's research and development programs are designed to offer hope to patients by developing safe and effective therapeutic candidates that have the potential to extend survival while maintaining quality of life. Maxim's lead drug candidate Ceplene(TM) (histamine dihydrochloride) is designed to prevent or inhibit oxidative stress, thereby reversing immune suppression and protecting critical immune cells. In November 2003, Maxim filed an application for market authorization in Europe for approval to market Ceplene for the treatment of advanced malignant melanoma. Ceplene is currently being tested in Phase 3 cancer clinical trials for advanced malignant melanoma with liver metastasis and acute myeloid leukemia. Phase 2 trials of Ceplene are also underway for the treatment of hepatitis C and advanced renal cell carcinoma. Maxim is also developing an oral formulation of histamine for the potential treatment of chronic liver diseases. More than 2,000 patients have participated in 17 completed and ongoing clinical trials of Ceplene. In addition to Ceplene, Maxim is developing small-molecule inhibitors and activators of programmed cell death, also known as apoptosis, which may serve as drug candidates for cancer, cardiovascular disease and other degenerative diseases. Ceplene, the MX116407, MX2105 and MX90745 series of compounds, and the apoptosis inducers are investigational drugs and have not been approved by the U.S. Food and Drug Administration (FDA) or any international regulatory agency. This news release contains certain forward-looking statements that involve risks and uncertainties. Such forward-looking statements include statements regarding the efficacy, safety and intended utilization of Ceplene, the oral histamine formulation, the MX116407, MX2105 and MX90745 series of compounds and the apoptosis inducers, and the conduct, results and timelines associated with the Company's clinical trials. Such statements are only predictions and the Company's actual results may differ materially from those anticipated in these forward-looking statements. Factors that may cause such differences include the risk that products that appeared promising in early research and clinical trials do not demonstrate safety or efficacy in larger-scale clinical trials, and the risk that the Company will not obtain approval to market its products. These factors and others are more fully discussed in the Company's periodic reports and other filings with the Securities and Exchange Commission. Note: The Maxim logo is a trademark of the Company. Editor's Note: This release is also available on the Internet at http://www.maxim.com. Contacts: Larry G. Stambaugh Aline Schimmel (Investors) Chairman, President and CEO Burns McClellan Anthony E. Altig (212) 213-0006 Chief Financial Officer Sean Collins (Media) (858) 453-4040 Valerie Bent (Media) CCG Investor Relations (818) 789-0100 ------------------------------------------------------------ This information was brought to you by Waymaker http://www.waymaker.net The following files are available for download: http://www.waymaker.net/bitonline/2004/03/30/20040330BIT00030/wkr0001.doc http://www.waymaker.net/bitonline/2004/03/30/20040330BIT00030/wkr0002.pdf