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AOD-9604 Pharmacokinetics & Metabolism Absorption & Distribution AOD-9604 exhibits unusual pharmacokinetic properties for a peptide, demonstrating activity via multiple administration routes in preclinical models: Oral bioavailability confirmed in pig and rodent studies, an uncommon characteristic for peptide compounds Rapid systemic distribution following intraperitoneal administration in mice (15-30 minutes) Following IV administration in pigs, AOD-9604 and degradation fragments appeared rapidly in plasma Oral administration showed slower kinetics but similar degradation product profiles Distribution studies using radiolabeled peptide (C-14-AOD9604) in rats revealed: Elevated concentrations in pineal body and thyroid tissues Distribution to all non-CNS tissues examined Minimal penetration of blood-brain barrier Tissue-specific accumulation patterns suggesting potential targeting mechanisms Metabolism & Elimination The metabolic fate of AOD-9604 involves rapid degradation through sequential N-terminal amino acid removal,: Plasma half-life of approximately 3 minutes following IV administration in pigs (compared to 21 minutes for full-length growth hormone) Sequential amino-terminal truncation represents the primary degradation pathway Principal metabolites identified in vivo include -2 amino acid and -3 amino acid fragments These truncated fragments retain some reduced in vitro anti-lipogenic activity A significant pharmacokinetic paradox exists: despite rapid plasma clearance (peptide undetectable at 56 minutes in spiked plasma studies), biological effects on body weight and fat metabolism persist for hours to days

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J Biol Chem 280:4217242180

There are many B12 deficiency signs and symptoms, including: Numbness Tingling, pins and needles Weakness, dizziness High homocysteine, low methionine Megaloblastic macrocytic anaemia Mild or moderate leukopenia (low white blood cells) Mild or moderate thrombocytopenia (low platelets) Enlarged red blood cells (macrocytosis) Abnormal white cell (neutrophils) Chronic fatigue or tiredness General weakness or lethargy General Signs and Symptoms: Ataxia, (unsteady walking) Paresthesia (prickling sensation) and weakness in peripheral nerves Confusion Infertility Vision loss Leg pains Shortness of breath Loss of appetite/weight loss Epigastric pain Osteoporosis Increased susceptibility to infection Failure to thrive in infants Vitiligo Premature greying of hair Burning feet Mental Changes Depression (including postpartum depression) Irritability Apathy Psychosis Sleepiness Suspiciousness (paranoia) Personality changes Memory loss Dementia, intellectual deterioration Hallucinations Violent behaviour Developmental delay and/or autistic behaviour in children Neurological signs and symptoms Abnormal sensations ie: pain, tingling, numbness of legs, arms, trunk A diminished sense of touch, pain and/or temperature Loss of position sense (awareness of body position) Weakness of limbs Clumsiness Tremor Symptoms mimicking Parkinsons disease or MS Spasticity of muscles Incontinence (urine or stool) Paralysis Vision changes Damage to the optic nerve neuritis, inflammation, atrophy Vascular Problems Transient ischemic attacks (TIAs) Cerebral vascular accident Coronary artery disease Myocardial infarction Congestive heart failure Palpitations Orthostatic hypotension Deep vein thrombosis Pulmonary embolism 7 Why is B12 deficiency often underdiagnosed

Common Misconceptions Retatrutide is proven to beat cagrilintide No head-to-head trial exists, so proven to beat is not a statement the evidence can support