a Phase 2 prostate cancer clinical trial is ongoing. Table 2: Squalamine vs Standard-of-care literature

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1 PRODUCT FACT SHEET Spring 2007 MISSION STATEMENT Genaera Corporation is a biopharmaceutical company with a focus on metabolic and respiratory diseases. The compounds in the Genaera pipeline address signal transduction pathways at the cellular level to treat a number of challenging diseases. These compounds hold promise as potential medical breakthroughs in asthma, obesity and diabetes. Genaera has made a strategic decision to out-license its non-core assets, including. CONTACT Genaera Corporation 5110 Campus Drive Plymouth Meeting, PA Ph: Fax: Investor Relations: Wed: Henry Wolfe, Ph.D. Executive Vice President and Chief Scientific Officer (610) This Product Fact Sheet contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks and uncertainties, known and unknown. Forward-looking statements reflect management's current views and are based on certain expectations and assumptions. You may identify some of these forward-looking statements by the use of words in the statements such as anticipate, believe, continue, develop, expect, plan and potential or other words of similar meaning. Genaera s actual results and performance could differ materially from those currently anticipated and expressed in these and other forward-looking statements as a result of a number of risk factors, described more fully in Genaera s filings with the U.S. Securities and Exchange Commission, all of which are available from the Commission in its EDGAR database at or on the Company s website Lactate: lactate is an intravenously administered anti-angiogenic agent developed for the treatment of solid tumors. A Phase 2 clinical trial is ongoing in prostate cancer. Several Phase 2 trials have been conducted in advanced NSCLC and ovarian cancer patients. The active ingredient (squalamine) is a small molecule produced synthetically with an excellent cost of goods. CLINICAL STUDIES Multiple Phase 1 dose ranging studies have been conducted in advanced cancer patients at multiple sites. The drug was generally welltolerated, with reversible hepatic transaminases elevation at higher dose levels and frequency. Several small phase 2 clinical studies have been conducted in advanced (stage III or IV) ovarian cancer and nonsmall cell lung cancer (NSCLC) patients, a Phase 2 prostate cancer clinical trial is ongoing. Table 1: Oncology Study results SQUALAMINE vs. STANDARD-OF-CARE LITERATURE Clinical results obtained with squalamine in non-small cell lung cancer patients are promising (Table 1). The definitive study in this field is a study by Schiller, et al (1) which compared four different treatment regimens in a randomized study of 1155 stage IIIb and IV NSCLC patients. As seen in Table 2, the results for (Herbst, et al (2) ) showed slightly more promising response rates, but were comparable to those reported by Schiller (1). Table 2: vs Standard-of-care literature Response Ovarian 1 NSCLC 2 NSCLC 3 Complete 19% 0% 2% Partial 15% 28% 22% Stable 38% 19% 49% Progression 27% 53% 27% 1 Continuous 5-day squalamine (200 mg/m2/day) infusion with carboplatin (AUC = 6), every 3 weeks, x6 2 Continuous 5-day squalamine infusion (300 mg/m2/day) following carboplatin (AUC = 6) and paclitaxel (225 mg/m2/day), every 3 wks, x6 3 Weekly squalamine (100 or 200 mg/m2) infusion with carboplatin (AUC = 2) and paclitaxel (75 mg/m2), x12 Herbst Schiller Patients (similar eligibility 35 evaluable 290 evaluable criteria ) * Paclitaxel Day 1 = 225 mg/m 2 Day 1 = 225 mg/m 2 Carboplatin Day 2 = AUC = 6 Day 2 = AUC = 6 Day 2-6 at mg/ m 2 /day Rest between cycles 21 days 21 days Cycles Response Rates 34 % overall 17 % overall Complete Response 0 % < 1 % Partial response 28 % 16 % Stable 19 % 23 % Disease Progression 53 % 49 % Could not be determined 0 % 11 % Median Survival 8.5 months 8.1 months 1 year survival 33 % 34 % * For both studies, similar eligibility criteria were used for stage IIIB and IV NSCLC patients.

2 PRECLINICAL ACTIVITY Anti-angiogenic activity has been demonstrated in several solid tumor xenograft models, which lead to the clinical development of squalamine in oncology. LUNG CANCER XENOGRAFT Effect of combination chemotherapy Nude mice bearing the MV-522 human lung tumor were treated for days 1 5 with vehicle (5% dextrose in water; t) or with paclitaxel (10 mg/kg/day, q.d. for 5 days) and carboplatin (20 mg/kg/day, q.d. for 5 days; r, X). Some treatment groups (, X) received squalamine (20 mg/kg/day) on days 1 5 and 8 9. Error bars, SE; hatched box, squalamine dosing period. (2) Vehicle Paclitaxel and Carboplatin Paclitaxel, carboplatin and squalamine Ovarian Cancer Xenograft CAOV3 ovarian cancer cells were inoculated subcutaneously in nude mice. After 7 days, animals with tumors of comparable size were randomized to treatment with control solution, squalamine (2 mg/kg on days 1 ± 10), cisplatin (4 mg/ kg on day 1), or cisplatin administered in combination with squalamine. Tumor volumes (mm3) are expressed as mean+s.e.m. for measurements to assess tumor growth delay due to the several treatments. (3) Tumor Volume (mm 3 ) /Cis-Plat 200 Cis-Platin Control Time, Months Page 2 of 5

3 MECHANISM OF ACTION: ANTI-ANGIOGENIC Unlike other treatments for anti-angiogenic therapies, squalamine does not interfere with the binding of VEGF to its receptor on proliferating endothelial cells. is a potent small molecule that works INSIDE these actively growing cells to specifically block the multiple intracellular pathways generated by the binding of VEGF and PDGFβ to their respective receptors. is rapidly eliminated from the systemic circulation (t 1/2 = 7.5 hours in humans), but retained in its intracellular site of action for more than 5 days. We believe this may be a key to the excellent safety observed with squalamine in clinical studies to date. Once inside the cell, exerts a number of effects which prevent activation of the p38 inflammatory pathway as well as VE-cadherin and α v β 3 and their downstream signaling pathways. This multi-faceted inhibition of intracellular pathways converts the actively proliferating endothelial cells into a dormant, normal vasculature, slowing tumor growth. lis a systemically administered anti-angiogenic drug being tested for the treatment of wet AMD. Unlike other treatments for wet AMD, squalamine does not interfere with the binding of VEGF to its receptor on proliferating endothelial cells. squalamine works INSIDE these actively growing cells to block the intracellular signals generated by the binding of VEGF and PDGFβ to their respective receptors. squalamine is rapidly eliminated from the systemic circulation (half-life = 7.5 hours in humans), but retained in its intracellular site of action for more than 5 days. Once inside the cell, squalamine exerts a number of effects which prevent activation of the p38 inflammatory pathway as well as VE-cadherin and ανβ3 and their downstream signaling pathways. This multi-faceted inhibition of intracellular pathways converts the actively proliferating endothelial cells into a more normal vasculature (Figure 1) Figure 1: EVIZON Mechanism of Action (blue dots) enters endothelial cells inhibits angiogenesis and inflammatory pathways (inhibits activities of MAPK, p38, a v β 3, and VE cadherin) No enos inhibition Page 3 of 5

4 SQUALAMINE AND HYPERTENSION The Competition: Anti-VEGF therapies, such as Avastin, block all intracellular downstream VEGF pathways, including enos, an enzyme which helps maintain normal blood pressure (Figure 2). As a result, administration of Avastin has been associated with clinically significant increases in blood pressure in patients. :, however does not block all intracellular VEGF pathways in proliferating endothelial cells, but rather only blocks specific pathways, such as the MAP kinase proliferative pathway, the p38 inflammatory pathway, as well as VEcadherin and α v β 3 and their downstream signaling pathways. A key difference in the mechanism of is that it does not block enos activity (Figure 2). Figure 2: does not inhibit enos activity % Maximum Response 100% 75% 50% 25% No inhibition by EVIZON Avastin inhibits enos (p<0.001) 0% Control VEGF EVIZON +VEGF Avastin +VEGF Page 4 of 5

5 We believe this mechanistic difference with will have a profound impact on patient safety. A Preliminary analysis of patients treated with squalamine in our Phase 2 wet AMD studies provides a first look at this effect. As seen in Figure 3, treatment of wet AMD patients with up to 40 mg of squalamine is not associated with clinically significant increases in systolic and diastolic blood pressure. Figure 3: Preliminary Analysis of Blood Pressure in wet AMD Patients treated with squalamine 10 5 Mean Change from Systolic Diastolic -15 N = 17 N = 26 N = 81 * 4 to 29 weeks of intravenous therapy REFERENCES Schiller JH, Harrington D, Belani CP, Langer C, Sandler A, Krook J, Zhu J, Johnson DH 2002 Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer. N Engl J Med 346:92-98 Herbst RS, Hammond LA, Carbone DP, Tran HT, Holroyd KJ, Desai A, Williams JI, Bekele BN, Hait H, Allgood V, Solomon S, Schiller JH 2003 A phase I/IIA trial of continuous five-day infusion of squalamine lactate (MSI-1256F) plus carboplatin and paclitaxel in patients with advanced non-small cell lung cancer. Clin Cancer Res 9: Li D, Williams JI, Pietras RJ 2002 and cisplatin block angiogenesis and growth of human ovarian cancer cells with or without HER-2 gene overexpression. Oncogene 21: McLane, et al, Angiogenesis Foundation 4th Annual International Conference Antiangiogenesis, New Frontiers in Therapeutic Development. Boston, MA. October 2006 Page 5 of 5

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