Celtic Therapeutics invests in continued development of SG2000, while Ipsen passes rights back to Spirogen.

Private equity firm Celtic Therapeutics is investing £15 million (about $24.13 million) in the continued clinical development of U.K.-based Spirogen’s DNA minor groove-binding anticancer drug, SG2000 (previously SJG-136). Spirogen separately announced that it regained worldwide development rights to the drug from Ipsen.

The company says that NCI-sponsored multicenter Phase II trials in ovarian and hematological cancers are expected to start in the near future.

The revised agreement with Ipsen completely supersedes the companies’ original 2003 deal. Thus Spirogen has full responsibility for global clinical development and commercialization of SG2000 either as a single agent or as combination therapy.

Spirogen also gets an exclusive, worldwide license to specific Ipsen IP covering pyrrolobenzodiazepines in combination with cytotoxic agents. On commercialization of SG2000, Ipsen will be eligible to receive royalties and commercial milestones. The company also retains a minority shareholding in Spirogen.

In addition to Celtic Therapeutics investment, the firm’s pharmaceutical development team will actively support the SG2000 program. Development to date has benefited from $20 million in investments including clinical trials sponsored by Cancer Research UK and the U.S. NCI under a CRADA.

Spirogen claims SG2000 has a novel mechanism of action that differentiates it from conventional cytotoxic and cross-linking agents. The company explains that adducts produced by chemotherapies such as cisplatin and melphalan result in a variety of recognizable distortions in the DNA double helix, and most of these adducts are recognized and removed by nucleotide excision repair (NER) factors.

In contrast, cross-links formed by SG2000 do not distort the DNA double helix and so are able to slip under the radar of NER. As a result, the company suggests SG2000 is highly active in refractory tumors, especially those where NER mechanisms are up-regulated, which can lead, for example, to cisplatin resistance.

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