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Examining GHS-R1a constitutive activity, receptor desensitisation and resensitisation kinetics, and the pharmacological consequences of selective GHS-R1a activation in peripheral tissues including cardiac, hepatic, and immune cell models where distinguishing GHS-R1a-specific from prolactin and cortisol-mediated biology is critical for mechanistic interpretation

Consequently, the use of FSP1 inhibitors combined with ferroptosis-inducing therapies is recommended for treating KRAS-mutant cancers, including PDAC [77]

But the additional GIP receptor binding domain makes tirzepatide a fundamentally different pharmacological tool

These differences were reported for all parameters investigated (Kalidindi et al., 2024)

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