What is 3HOTP?

A New Paradigm in Obesity Treatment

• 3HOTP is a first-in-class, vaccine-like peptide drug targeting Apolipoprotein B100. It uniquely combines durable weight maintenance after weight loss with additional metabolic and anti-inflammatory benefits, all without GI, hepatic, vascular, or neuropsychiatric side effects. This differentiated profile aligns with the FDA’s latest draft guidance that weight regulation should be accompanied by broader metabolic improvements. With its novel immune-therapeutic mechanism, extended dosing intervals, and superior safety outlook, 3HOTP offers clear advantages beyond the crowded GLP-1 market and addresses a wider patient population. We are seeking a technology transfer partnership to advance 3HOTP through Phase 1a/1b trials (planned for early 2026), leveraging a robust design to deliver compelling proof-of-concept and a clear regulatory path to market.

3HOTP for Human & Animal

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  1. Vaccination

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  2. Stimulation of B cells

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  3. Induction of antibodies

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  4. The induced antibodies bind to ApoB100

Therapeutic principle and approach

• When 3HOTP is administered, antibodies form that recognize the antigenic peptide OTP5 (the active pharmaceutical ingredient of 3HOTP).
• These antibodies bind to the ApoB100 protein of lipoproteins (VLDL, IDL, LDL).
• The Fab domains (two) of the antibodies bind to the ApoB100 of the fat particles, preventing fat storage in adipocytes.
• The Fc domain (one) of the antibodies promote the phagocytic uptake of the antibody-bound fat particles by macrophages.

Mode of Action I

Mode of Action II

• When LDL is oxidized into oxLDL, it is captured by scavenger receptors of macrophages, transforming them into foam cells (diseased cells).
• However, antibody-bound lipid particles bind to Fc receptors of macrophages before being oxidized, and the lipid particles are absorbed and degraded by macrophages, without converting them into foam cells.

ApoB100 as an immunotherapeutic target

In adipose tissues

• Re-routing of (V)LDL towards macrophages (no foam cells)
• Increased lipolysis
• A less inflammatory environment

In liver

• Blockage of lipid uptake by hepatocytes

Secondary beneficial effects

• Tissue macrophage repolarization towards a non-inflammatory phenotype.
• Prevention of the onset and progression of diet-induced fatty liver, type 2 diabetes mellitus (T2DM), and most likely atherogenesis.