Strategically focused on identifying small molecule drugs that have a proven history of efficacy

Lantern’s AI-enabled approach identifies abandoned or shelved small-molecule drugs that have a proven history of safety, some of which have shown efficacy in clinical trials. Lantern develops each drug in its pipeline by using an efficient and thorough workflow to advance each drug to become a precision medicine treatment to the patient quickly and at a low cost. Lantern’s development workflow includes pre-clinical studies where drug efficacy and gene signatures are identified through strategic collaborations with some of the top academic institutions and clinical translational centers in the world. Using this collaborative and innovative approach, Lantern is ensuring that each of the drugs in its pipeline is being developed to treat the right patients with the right drug. 

Lantern Pharma Oncology Drug Portfolio



LP-100 Chemical Structure

Mechanism of Action

LP-100 is a non-hormone, non-chemotherapy, DNA Damage Repair (DDR) inhibitor. It shows multiple cytotoxic effects on tumor cell biology such as DNA adduct formation, RNA polymerase stalling and redox protein modification.

Background

LP-100 was first developed by MGI. Pharma and later in collaboration with global pharma company, Eisai.  After achieving an objective response rate in 12-15% of prostate and ovarian cancer patients in phase 2 and phase 3 clinical trials, the program was shelved. Irofulven has been in over 30 clinical trials with 900 patients treated and has a history of tolerability, safety and efficacy in certain tumor sub-types. Lantern’s process was to uncover a genomic signature that determines potential responders, develop suitable preclinical data, and successfully out-license it to Oncology Venture (a European Biotech) in 18 months.

LP-300 Chemical Structure

Mechanism of Action

LP-300 is a first-in-class combination agent indicated in non-small cell lung cancer. With chemoprotective and chemosensitizing activity, LP-300 has potential as a combination agent or adjuvant in front line, second line or salvage therapy in newly diagnosed, relapsed, metastatic or advanced NSCLC for overall survival enhancement and toxicity alleviation from primary chemotherapy or standard of care. LP-300 shows cysteine modifying activity on select proteins (ALK), and has shown that it modulates protein function (EGFR, MET, and ROS1). It also acts as a chemo-sensitizer for combination therapies by inactivating proteins that are modulating cellular redox status and drug resistance (TRX, GRX) and possesses chemoprotectant activity that reduces toxicities associated with Taxane / Platinum based chemotherapies. LP-300 has great promise to be used synergistically with various treatment regimens including chemotherapy, targeted therapy and immunotherapy combinations by virtue of its multi-modal mechanism of action, capacity to counter multi-drug resistance, and statistically significant survival outcomes in subgroups in previous clinical trials when combined with standard of care.

Background
LP-300 has been in 4 major clinical trials with over 600 patients that were treated with demonstrable safety, and tolerability, but also with efficacy in certain patient populations. LP-300 in combination with Cisplatin and Paclitaxel demonstrated significant benefit in female non-smokers with advanced NSCLC adenocarcinoma. Although the phase 3 trial failed to achieve overall clinical efficacy, it did achieve (in retrospective analysis) overall survival (OS) of 25 months, with a 2-year survival rate of 51.4%, in females with advanced adenocarcinoma of the lung. These female cancer patients were uniformly receiving both paclitaxel/cisplatin and LP-300.

LP-184 Chemical Structure

Mechanism of Action

LP-184 is a non-hormone, non-chemotherapy, next-generation DNA Damage Repair (DDR) inhibitor. Indicated primarily in solid tumors such as prostate, ovarian, liver and thyroid cancers, LP-184 is a next generation analog of Irofulven. Developed through combinatorial chemistry and screened against conventional therapies both in vitro and in vivo with superior performance, LP-184 cytotoxicity is mediated through the Transcription Coupled Nucleotide Excision Repair (TC-NER) pathway, via alkylation of DNA leading to cell cycle arrest in S phase. Additional cytotoxic effects on tumor include generation of reactive oxygen species, chemical modification of various intracellular proteins, and induction of the MAPK pathway followed by apoptosis.

Background

LP-184, demonstrates highly improved anti-tumor efficacy, tumor regression in a xenograft model of multidrug resistant cancer, therapeutic index, and bioavailability and clearance.

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