You seem to be doing quite well on whatever you’re taking at the moment. Lumateperone might not even work out for you. It’s still going to be the same old story about some meds not working for some people. It’s not guaranteed to work for everybody.
Also 3 years will show up whether or not it’s harming people.
Mechanism of Action
The mechanism of action of lumateperone in the treatment of schizophrenia is unknown. However, the efficacy of
lumateperone could be mediated through a combination of antagonist activity at central serotonin 5-HT2A receptors
and postsynaptic antagonist activity at central dopamine D2 receptors.
Animal Toxicology and/or Pharmacology
Oral administration of lumateperone caused systemic intracytoplasmic accumulation of pigmented material in dogs,rats, and mice at clinically relevant exposures (AUC). Intracytoplasmic pigmentation appeared to be localized in lysosomes. Accumulation of pigmented material persisted without reversal at the end of 1- to 2-month drug-free periods. Pigmented material was observed in the brain and spinal cord of all three species, and in the heart and eye of rats. Although the composition of the pigmented material was not established, the material is likely polymers or protein adducts formed from aniline
metabolites of lumateperone.In the dog, accumulation of pigmented material in the brain and spinal cord was associated with neuronal degeneration and necrosis, followed by axonal degeneration and histiocytic inflammation after oral administration of lumateperone for up to 9 months. In the rat, accumulation of pigmented material was associated with degenerative changes and signs of an inflammatory response in the spinal cord, peripheral nervous system, eye, and heart after
oral administration of lumateperone for up to 2 years. Although overt degenerative changes were not observed in the rat brain, the presence of pigment-containing infiltrating macrophages is consistent with an inflammatory response. The role of intracytoplasmic pigmented material in causing these lesions was not definitively established; however, the colocalization of pigmented material in tissues with degenerative changes and signs of inflammation is supportive. Alternatively, the aniline metabolites of lumateperone may undergo metabolic activation forming reactive metabolites that contribute to the observed toxicities. The role of intracellular accumulation of lumateperone or its non-aniline metabolites in these toxicities could not be ruled out. The aniline metabolites thought to be responsible for these toxicities were detected in dogs and rats but were not present in humans at quantifiable levels. Based on all the available evidence, these toxicities do not appear to be relevant to humans
With long-term administration, the most frequent (occurring in ≥ 5% of patients) treatment-emergent adverse events, regardless of whether such adverse event was related to treatment, were decrease in weight (9.5%), dry mouth (7.6%), diarrhea (7.0%), and headache (5.1%). The proportion of patients experiencing motor side effects while on lumateperone was low: any adverse event related to extrapyramidal side effects combined including akathisia (5.3%); and akathisia specifically (0.5%). There were no signs of treatment-emergent extrapyramidal side effects, akathisia, or dyskinesia as measured by the Simpson Angus Scale (SAS), the Barnes Akathisia Rating Scale (BARS), or the Abnormal Involuntary Movement Scale (AIMS), respectively. In addition, there were no signs of treatment-emergent suicidal ideation or behavior as measured by the Columbia-Suicide Severity Rating Scale (C-SSRS).
But of course, side effects is a must in APS, we are schizophrenic after all. Ill give it a try when ill get the chance. And reading those ‘‘side-effects’’ its not so bad.
Possibly relevant to some: Says you aren’t supposed to take it with modafinil, valproate or fluvoxamine. (Plus some others but those seemed most relevant).