The Sixpeaks Bio Approach

Protection of Lean Tissue Mass will be a Core of Future Healthy Weight Loss Solutions

Future therapies will do better

Losing Skeletal Muscle Mass undermines the health benefits of weight loss, weight cycling causes unfavorable loss of skeletal muscle. The magnitude of lean tissue mass loss is predictive of recurrent weight gain. Preserving or expanding skeletal muscle during periods of negative energy balance is bound to reduce subsequent risk of weight regain, moreover it improves glucose and lipid metabolism.

Comparison of therapies with regard to muscle mass reduction

The ‘Healthy weightloss’-regime

Successful implementation of negative energy balance is achieved with clinically proven satiety inducing GLP-1 agonists. Combination with muscle expanding activin 2A/B receptor blockade accelerates loss of fat mass whilst preserving metabolically active muscle fibers.

Incretin-based appetite suppressant with simultaneous fat cell reducer and muscleexpander

Placing the Muscle at the Center of Future Diabetes and Weight Management

  • GDF8/myostatin pathway controls skeletal muscle mass
  • Targeting this pathway leads to increased muscle mass – effects on muscle strength has been disappointing, but increased muscle mass leads to improved glycemic control/metabolic fitness

  • Appetite suppressant incretins are established Standard of Care (SoC)
  • Adding ActR2A/B blockade to semaglutide or tirzepatide completely prevents incretin induced lean tissue mass loss
  • The ideal conduit to healthy weight loss

  • High-affine, fully human antibody, monthly dosing possible
  • Modality as well as pathway clinically derisked from exposure of more than 1000 patients
  • Next generation multi-specificity mAbs provides option for superior therapeutic utility and targeting of patient subgroups

Simultanously addressing comorbidities:

  • Restoring or preserving cardiac function in heart failure
  • Improving glycemic control in type 2 diabetes (T2D)
  • Addressing muscle wasting associated with weight cycling and T2 diabetes

Choice of modality determines therapeutic success

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Muscle fibers are equipped with activin IIA and IIB receptors (ActRIIA/B). These receptors act as a brake on muscle growth

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Continuous engagement of ActRIIA/B by endogenous ligands (eg. myostatin, activinA, activinB, GDF11) triggers cellular events reducing muscle function and metabolism. As we age, muscle health and function are increasingly halted through intensification of ActRIIA/B signaling.

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Pharmacological blockade of the ActRIIA/B signaling lifts the brake on muscle growth with resulting hypertrophy and improved glucose handling. The most effective pharmacological means to dampen ActRIIA/B signaling is through direct receptor blockade.

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Pharmacological blockade of individual ligands is a far more complex task as it requires concomitant application of a cocktail of ligand specific antibodies of invention of multispecific ligand neutralizing antibodies. Blocking the joint ActRIIA/B receptors is bound to be the most efficacious way to trigger muscle hypertrophy.

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Generic class proposal:
Inhibitor of the activin receptor signaling pathway (IASP)

Leveraging the power of designed polypharmacology

While we envisage our best-in-class program as a standalone medicine as well as combo therapy, we further advance our molecules by dialing in complementary pharmacology, such as GLP-1 agonism. We achieve this by conjugating e.g. GLP-1 receptor activating peptides to our Activin targeting antibodies, so-called “antibody peptide conjugates (APCs)”.
GLP-1 peptide (yellow) chemically linked to our Activin receptor targeting Antibody

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