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Biotech / Medical : Ligand (LGND) Breakout! -- Ignore unavailable to you. Want to Upgrade?

To: Robert L. Ray who wrote (22745)	6/26/1998 4:19:00 PM
From: jayhawk969	Respond to of 32384

Robert, Welcome aboard the train. A lot of today's volume was at the end of the day. It may dip again next week but my gut is we have more upside exposure that downside exposure. SRGN is correspondingly moving up its bid and ask.

To: Robert L. Ray who wrote (22745)	6/26/1998 5:36:00 PM
From: Henry Niman	Respond to of 32384

Robert, Welcome aboard and thanks for the heads up on the addition indications for the various sex hormones. Actually, several of the SERMs are in the clinic, but LGND really has a discovery role in these areas. Evista (Raloxifene has already been approved for osteoporosis and is just beginning a breast cancer prevention trial going head to head with Tamoxifen, another SERM that has been approved for some time for treating breast cancer. LGND's Rexinoids (Targretin in advanced Phase III trials for CTCL and LGD1269 and LGD1324 are ready for the clinic) synergize with both SERMs and part of the LLY deal is to look at combining Rexinoids with SERMs (LLY has second generation compounds also) to treat breast cancer (and of course they also synergize to prevent breast cancer). LGND has helped identify several additional SERMs that are in the clinic. With PFE they identified Droloxifene and CP-366,156 for treating and preventing osteoporosis and with AHP (as you know they make the $1 Billion drug Premarin), they have identified TSE424 for osteoporosis which has also entered the clinic. Another SERM is ready to enter the clinic for the treatment of breast cancer. Thus, LGND has many compounds in the SERM area, but all are partnered out. These compounds are laying the groundwork for use in treatment and prevention applications for huge markets. Most interesting for LGND shareholders are the somewhat younger programs using designer progestins and designer androgens. These compounds also target huge markets and the animal data is compelling. Moreover, LGND owns most of the rights. they do have a progesterone program with AHP, but they own all of the androgen program and these compounds are proprietary and being aggressively developed by the largest androgen group in the world. This thread of course has more than its share of noise, but investors looking long term should be extremely pleased by what they see, as well as by what is anticipated. In 1996 BARS initiated coverage with a 10 year projection of $14.55 EPS by 2006.

To: Robert L. Ray who wrote (22745)	6/26/1998 7:58:00 PM
From: bluejeans	Read Replies (1) \| Respond to of 32384

Hi Robert, I've been mostly a lurker here forever, and today I finally took the plunge and bought in. I hope you learned the Ligand handshake while being a lurker;) Bob BTW: Do you still have the other 2 stocks you bought on Oct. 1?

To: Robert L. Ray who wrote (22745)	6/29/1998 7:31:00 AM
From: Henry Niman	Respond to of 32384

Here's one of the abstracts for talks at the International AIDS conference for topical Panretin (notice the p value for the PGA response) [619/22283] North American phase 3 study (protocol L1057T-31) of panretinT gel (LGD1057, ALRT1057) for cutaneous aids-related Kaposi's sarcoma Alvin Frie Dman-Kien1 2 M. Conant3 . 1New York University, Dept. of Dermatology 550 First Street, New York, NY; 2New York University Medical Center New York NY; 3Private Medical Practice San Francico CA, USA Background: A Phase 3, multicenter, randomized, double blind clinical trial was conducted to evaluate the safety, cutaneous tolerance and anti-tumor effects of PANRETIN (9-cis-retinoic acid) Gel in patients with AIDS-related Kaposi's sarcoma (KS). Methods: HIV-positive patients with biopsy proven KS were randomized to topical PANRETIN 0.1% Gel or vehicle gel, with intended treatment at least 12 weeks, starting TID advancing to QID. Six index cutaneous lesions and other parameters were assessed at least every four weeks. Results: 35 US and 3 Canadian study centers enrolled 266 male and 2 female patients. Treatment arms (PANRETIN Gel vs. vehicle gel) were well matched for age, ethnicity, gender, time since KS diagnosis, Karnofsky status, history of opportunistic infections, KS lesions, presence of visceral KS, baseline CD4 count (median 154 vs. 144 cells/mm3), % receiving prior systemic (36% vs. 34%) and prior topical/local (49% vs. 53%) anti-KS therapy, and % receiving concurrent antiRetroviral (ARV): any ARV (93% vs. 93%), 3 or more ARV (72% vs. 79%), and protease inhibitor (74% vs. 82%). The overall response (complete or partial) rate determined by applying AIDS Clinical Trial Group (ACTG) criteria to each patient's 6 index lesions was 35% (47/134) for PANRETIN Gel vs. 18% (24/134) for vehicle patients (p = 0.002). The cumulative response rate for all patients treated with PANRETIN Gel including the follow-on, open label phase was 49% (90/184). One patient had complete clearing of all index lesions on PANRETIN Gel. While responses for the vehicle arm patients correlated with the degree of ARV therapy, after adjusting for concurrent ARV therapy the response rate for PANRETIN Gel was still substantially higher than for vehicle. The Physician's Global Assessment (PGA) responses were substantially higher for PANRETIN Gel vs. vehicle (p = 0.000003). Response according to ACTG criteria was strongly corroborated not only by PGA, but also by the patient quality of life responses. PANRETIN Gel-related adverse events were nearly exclusively confined to the site of application, with the most frequent consisting of rash (72% incidence), pain (32%) and pruritus (13%). Conclusions: PANRETIN Gel produced responses according to ACTG criteria in nearly 50% of patients treated, and was statistically superior to vehicle gel in the initial blinded phase of study, even after adjusting for ARV therapy. Adverse events were nearly exclusively confined to the site of application and were generally easily manageable. PANRETIN Gel may provide a very tolerable, non-invasive, patient-controlled alternative to systemic chemotherapy for the treatment of cutaneous AIDS-related KS. Author-indicated categories: Choice 1: Track B Clinical Science and Care, HIV-related Diseases, Kaposi's sarcoma Choice 2: HIV-Associated Neoplasia Presentation Date, Time, Room: 02-Jul-98, 3:00P, Hall VII

To: Robert L. Ray who wrote (22745)	6/29/1998 7:35:00 AM
From: Henry Niman	Read Replies (2) \| Respond to of 32384

Here's the abstract on the halted International trial: [618/22277] Topical 9-cis-Retinoic acid (PanretinT) gel as treatment of cutaneous AIDS-related Kaposis sarcoma: Interim results of an international, placebo-controlled trial (ALRT 1057-503) Neil Bodsworth On Behalf of the International Panretin KS Study Group International. Taylor Square Private Clinic, 302 Bourke Street Darlinghurst NSW 2010, Australia Objective: To assess the efficacy and safety of Panretin 0.1% gel (9-cis-retinoic; Allergan Inc and Ligand Pharmaceuticals Inc.) as treatment of AIDS-related cutaneous Kaposis sarcoma (KS) lesions. Method: HIV-infected persons with <Picture>3 biopsy confirmed, cutaneous KS lesions and with no prior local treatment to indicator lesions nor prior systemic retinoids were eligible for this placebo-controlled, randomised (1:1 ratio), double-blind study of 0.1% 9-cis-retinoic acid gel. Gel or matching placebo vehicle was applied to lesions twice daily for 12-weeks or until lesions progressed (PD). Enrolment was at 17 sites in Australia, US and Europe. Response was assessed by measurement of lesions according to the ACTG KS criteria as applied to topical therapy for complete clinical response (CCR), partial response (PR) and progressive disease (PD) and with supportive photography. Target enrolment was 270. A single planned interim analysis was performed for the first 82 patients. Results: Accrual was ceased after the interim analysis showed a significant difference in treatment arms which met the trial's stopping rule (alpha < 0.005). Patients assigned active gel (n = 36) were significantly more likely than placebo assignees (n = 46) to respond (either CCR or PR) to treatment (41.7% vs 6.5%, p = 0.00027). Therapy was well tolerated with toxicity limited to local cutaneous irritation. Treatment arms (active vs placebo) were well matched for ethnicity, age, gender (all subjects were male), mean (ñ SE) CD4 cell count at baseline (197 ñ 29 vs 161 ñ 25), proportion receiving any antiRetroviral (ARV) therapy on study (95% vs 100%), any protease inhibitor (72% vs 87%) and any triple (or greater) ARV combination (78% vs 94%). Conclusion: In this international study, topical treatment of cutaneous KS lesions with 0.1% 9-cis-retinoic acid gel was associated with a six-fold improvement in response rate when compared to vehicle gel (42% vs 7%, p = 0.00027). Therapy was well tolerated with toxicity limited to local skin irritation. Author-indicated categories: Choice 1: Track B Clinical Science and Care, HIV-related Diseases, Kaposi's sarcoma Choice 2: Track B Clinical Science and Care, Organ Systems, Dermatological HIV-Associated Neoplasia Presentation Date, Time, Room: 02-Jul-98, 3:00P, Hall VII