Tag: NOVEL

  • Anavex 2-73 (Blarcamesine)

    Sigma-1 agonist + muscarinic modulator

    A sigma-1 agonist with muscarinic acetylcholine receptor activity; investigated for Alzheimer disease, Parkinson dementia, and Rett syndrome.

    Abstract

    Anavex 2-73 (blarcamesine, AVN-101; CAS 195615-83-9; molecular formula C16H21NO; molecular weight 243.34) is a multi-target sigma-1 agonist with muscarinic acetylcholine receptor activity, developed by Anavex Life Sciences. Sigma-1 affinity is approximately 860 nM (lower than cutamesine but functionally meaningful); the compound additionally interacts with muscarinic M1 and M2 receptors. Phase 2 trials in Alzheimer disease and Parkinson disease dementia demonstrated dose-dependent improvements in some cognitive endpoints. Phase 3 in Rett syndrome (EXCELLENCE trial) reported positive results in 2024 for select endpoints. Plasma half-life is approximately 14 hours. Used as a multi-target research compound for sigma-1 and muscarinic neuropharmacology.

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    FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

  • Thymopentin

    Plain-language summaryIntrigue 50 / 100

    Thymopentin is a 5-amino-acid synthetic peptide representing the active region of thymopoietin. Used historically for psoriasis and immune modulation. Not stocked by Kodiac. This monograph is provided for research and educational reference.

    Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

    Synthetic pentapeptide of thymopoietin

    A synthetic pentapeptide fragment (residues 32-36) of thymopoietin marketed in Europe and Asia for immunomodulation in chronic infections and autoimmune disease.

    Abstract

    Thymopentin (Timunox, TP-5; Arg-Lys-Asp-Val-Tyr; CAS 69558-55-0; molecular weight 679.78) is a synthetic pentapeptide corresponding to residues 32-36 of thymopoietin, a thymic hormone. The fragment retains the immunomodulatory activity of full-length thymopoietin. The compound is approved in Italy and several Asian countries for primary immunodeficiency, hepatitis B, atopic dermatitis adjunct, and autoimmune disease support. Mechanism includes T-cell maturation, NK cell modulation, and cytokine balance effects. Administered subcutaneously. Doses are 50 mg three times weekly in clinical use.

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    FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

  • BNN-27

    Plain-language summaryIntrigue 70 / 100

    BNN-27 is a synthetic neurosteroid derivative of DHEA developed at the BRFAA in Athens. It mimics nerve growth factor (NGF) without activating other DHEA pathways. Investigated for neurodegeneration. Not stocked by Kodiac. This monograph is provided for research and educational reference.

    Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

    Synthetic DHEA derivative / NGF mimetic

    A synthetic DHEA derivative (17-spiroepoxy DHEA) developed at Bionature E.A. Ltd as a selective TrkA agonist mimicking NGF activity.

    Abstract

    BNN-27 (17-spiro-(2′-amino-1′,3′-thiazolin-2-yl)-androst-5-en-3-beta-ol) is a synthetic DHEA derivative developed by Bionature E.A. Ltd (Greece) and Achilleas Gravanis’s group for selective activation of TrkA, the high-affinity NGF receptor. The compound is a microneurotrophin: it mimics the NGF/TrkA pathway without binding to the p75 neurotrophin receptor (NTR). Animal studies show neuroprotective effects in models of diabetic neuropathy, retinal degeneration, and Alzheimer disease. The compound has not advanced to large clinical trials. Pharmacokinetics: oral bioavailability is good (steroid scaffold). Sold as research peptide/compound.

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    FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

  • Beta-Phenylethylamine (PEA)

    Endogenous trace amine / TAAR1 agonist

    An endogenous trace amine; a TAAR1 agonist found at low concentrations in mammalian brain; structurally the parent of amphetamine.

    Abstract

    Beta-phenylethylamine (PEA; 2-phenylethylamine; CAS 64-04-0; molecular formula C8H11N; molecular weight 121.18) is an endogenous trace amine produced by decarboxylation of L-phenylalanine. The compound is found at low concentrations in mammalian brain (nM range) and in dietary sources including chocolate, cheese, and certain fermented foods. PEA is the prototype TAAR1 agonist (Ki approximately 700 nM at human TAAR1) with secondary effects on monoamine release and inhibition of MAO-B. Plasma half-life is extremely short (approximately 5 to 10 minutes) owing to rapid MAO-B-mediated degradation; exogenous oral PEA is therefore largely inactive without MAO-B inhibition (selegiline combination is used to extend duration). Behavioral and physiological effects parallel amphetamine but with shorter duration and lower potency. Used as the canonical endogenous TAAR1 agonist in trace amine research.

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    FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

  • NG2-101

    Plain-language summaryIntrigue 30 / 100

    NG2-101 is an investigational neurogenic peptide. Limited published research. Not stocked by Kodiac. This monograph is provided for research and educational reference.

    Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

    Investigational neurogenic peptide

    An investigational peptide for hippocampal neurogenesis with limited public characterization.

    Abstract

    NG2-101 is a research peptide marketed for neurogenic applications with limited published characterization. The compound’s specific sequence and mechanism are not fully disclosed in peer-reviewed literature; vendor claims center on hippocampal neurogenesis effects similar to BDNF or NGF mimetics. The absence of peer-reviewed characterization is significant; investigators should treat the compound with substantial skepticism and obtain analytical confirmation of identity and purity before any investigational use. There is no formal pharmacokinetic, safety, or efficacy data.

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    FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

  • 5-Amino-1MQ

    Plain-language summaryIntrigue 72 / 100

    5-Amino-1MQ is a small molecule that selectively inhibits the NNMT enzyme. NNMT degrades NAD+ precursors and methyl donors; inhibiting it boosts cellular energy and fat metabolism, with research interest in obesity and metabolic disease. Capsule format here. Stocked in the Kodiac catalog as a research-only powder for laboratory work; not a medicine, not for human consumption.

    Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

    Small-molecule selective NNMT inhibitor (capsule format)

    A 159 Da quinolinium small molecule that selectively inhibits nicotinamide N-methyltransferase, characterized for effects on adipose metabolism and skeletal muscle stem cell function. Supplied as 60 capsules x 50 mg.

    Abstract

    5-Amino-1-methylquinolinium iodide (5-Amino-1MQ; CAS 954126-98-8; molecular formula C11H12N2; molecular weight 159.20 for the cation; the iodide salt has additional mass) is a small-molecule selective inhibitor of nicotinamide N-methyltransferase (NNMT, EC 2.1.1.1), the enzyme that methylates nicotinamide to N1-methylnicotinamide using S-adenosylmethionine (SAM) as the methyl donor. NNMT activity diverts nicotinamide away from the NAD+ salvage pathway and consumes SAM, which connects NNMT activity to both the cellular NAD+ pool and the methylation potential of the cell. NNMT is overexpressed in many cancers (where it has been characterized as an “oncometabolic” enzyme) and in obesity-associated white adipose tissue, where it has been linked to insulin resistance and to the metabolic dysfunction phenotype. Selective NNMT inhibitors including 5-Amino-1MQ have been developed primarily by academic medicinal chemistry groups beginning in the late 2010s and have been characterized in cell culture, in vivo rodent obesity and aging models, and in skeletal muscle stem cell and aging models. The compound is supplied at Kodiac biolabs as a 60-capsule oral preparation, 50 milligrams per capsule, reflecting the small molecule’s stability and oral bioavailability. There is no FDA-approved IND for 5-Amino-1MQ in any indication. The compound is not a regulated drug substance in the United States, the European Union, or Japan. The principal limitations on the strength of the evidence are the relatively short duration of the published research record and the limited human safety and efficacy data.

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    FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

  • 9-Me-BC

    Plain-language summaryIntrigue 64 / 100

    9-Me-BC (9-methyl-beta-carboline) is a small molecule based on the beta-carboline scaffold. Research suggests it has dopaminergic neuroprotective effects, with potential implications in Parkinson disease research. Capsule format here. Stocked in the Kodiac catalog as a research-only powder for laboratory work; not a medicine, not for human consumption.

    Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

    Beta-carboline alkaloid, dopaminergic neuroprotective small molecule (capsule format)

    A 182 Da methylated beta-carboline alkaloid characterized for dopaminergic neuroprotective effects, increased dopamine neuron differentiation, and BDNF expression in animal models. Supplied as 30 capsules x 20 mg.

    Abstract

    9-Methyl-beta-carboline (9-Me-BC; CAS 2521-07-5; molecular formula C12H10N2; molecular weight 182.22) is a small-molecule beta-carboline alkaloid bearing a methyl substituent on the 9-position indole nitrogen. The compound is a member of the broader beta-carboline family, naturally occurring alkaloids found in trace concentrations in many plants (notably the harmal family of psychoactive plants used in traditional preparations) and present at low concentrations in mammalian tissues including human plasma. The synthetic 9-methylated variant has attracted research interest beginning in the 2010s for a distinctive pharmacological profile that combines dopaminergic neuroprotective effects, increased dopamine neuron differentiation in cell culture, and elevated BDNF expression in rodent brain. Unlike many psychoactive beta-carbolines (harmaline, harmine, others), 9-Me-BC has substantially reduced affinity for the monoamine oxidase A enzyme and substantially reduced psychoactive effects at the doses used in published preclinical work. The compound is supplied at Kodiac biolabs as a 30-capsule oral preparation, 20 milligrams per capsule, reflecting the small molecule’s stability and good oral bioavailability. There is no FDA-approved IND for 9-Me-BC in any indication. The principal limitations on the strength of the evidence are the relatively short duration of the published research record, dominance of a small number of laboratories (primarily in the German neuroscience research community), and the absence of human clinical data.

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  • SS-31

    Plain-language summaryIntrigue 88 / 100

    SS-31, also called elamipretide, is a four-amino-acid peptide that selectively targets the inner mitochondrial membrane. It binds cardiolipin (a unique mitochondrial lipid) and stabilizes the mitochondrial membrane during stress, with research interest in heart failure, kidney disease, and aging. Stocked in the Kodiac catalog as a research-only powder for laboratory work; not a medicine, not for human consumption.

    Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

    Synthetic tetrapeptide mitochondrial-targeting cardiolipin-binding peptide

    A 4-amino-acid mitochondrial-targeting peptide developed at Cornell University, characterized for binding to cardiolipin in the inner mitochondrial membrane and protecting mitochondrial function in oxidative stress.

    Abstract

    SS-31 (sequence D-Arg-Dmt-Lys-Phe-NH2, also known as elamipretide, Bendavia, MTP-131; CAS 736992-21-5; molecular formula C32H49N9O5; molecular weight 639.79) is a synthetic tetrapeptide developed in the laboratory of Hazel Szeto at Cornell University Medical College beginning in the early 2000s. The peptide is the most extensively characterized member of the Szeto-Schiller (SS) series of mitochondrial-targeting tetrapeptides. The biological mechanism is binding to cardiolipin in the inner mitochondrial membrane, which protects the membrane lipid environment from peroxidation, stabilizes the supercomplexes of the electron transport chain, and improves mitochondrial efficiency in conditions of oxidative stress or mitochondrial dysfunction. The compound is the active pharmaceutical ingredient in elamipretide (Bendavia), which has been advanced through Phase 2 and Phase 3 clinical trials by Stealth BioTherapeutics for primary mitochondrial myopathies, age-related macular degeneration (dry AMD with geographic atrophy), Barth syndrome, and other mitochondrial dysfunction indications. The clinical record is mixed; the most-promising results have come in Barth syndrome and primary mitochondrial myopathy. The compound is not approved by any regulatory authority for human or veterinary use as of this revision; recent FDA review in geographic atrophy resulted in a complete response letter requesting additional data. The Kodiac biolabs lot of record is SW260307, manufactured 7 March 2026 by Xian Sowu Biotech, with a vendor COA assay of 99.62 percent and a supplementary HPLC area-percent of 99.18 percent at 220 nm; both documents are archived on the lab results page.

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  • Dihexa

    Plain-language summaryIntrigue 87 / 100

    Dihexa is a small molecule based on a fragment of angiotensin (a blood pressure hormone). Despite that origin, what makes it interesting is what it does in the brain: research shows it dramatically increases the formation of new connections between brain cells (synapses), with potential applications in Alzheimer disease and cognitive enhancement. Stocked in the Kodiac catalog as a research-only powder for laboratory work; not a medicine, not for human consumption.

    Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

    Angiotensin IV analog (procognitive small peptidomimetic)

    A small angiotensin IV analog with a contested mechanism of action, a high-profile commercialization failure, and a literature record selectively retracted in 2025.

    Abstract

    Dihexa, also known as PNB-0408 and N-hexanoic-Tyr-Ile-(6) amino-hexanoic amide, is a hexapeptide-derived small molecule developed in the Harding laboratory at Washington State University as a procognitive analog of angiotensin IV. It was foundationally hypothesized to act through agonism of the hepatocyte growth factor (HGF) / c-Met receptor system, a mechanism that promised oral bioavailability, blood-brain barrier penetration at picomolar potency, and rapid synaptogenesis in cortical and hippocampal neurons. Between 2011 and 2014, four peer-reviewed publications established the compound’s commercial pipeline and underwrote the formation of Athira Pharma, a publicly traded biotechnology firm that raised over 204 million dollars in a 2020 initial public offering. Each of these four publications was retracted by the Journal of Pharmacology and Experimental Therapeutics in April 2025 following findings of academic misconduct, specifically the splicing and duplication of Western blot bands across distinct experimental conditions. The Department of Justice settled a False Claims Act qui tam action against Athira Pharma in January 2025 for 4.07 million dollars. The clinical lead derived from this program, fosgonimeton (ATH-1017, NDX-1017), failed to meet primary endpoints in the LIFT-AD Phase 2/3 trial in mild-to-moderate Alzheimer disease and the SHAPE Phase 2 trial in dementia with Lewy bodies. This monograph reviews what is now established about Dihexa’s chemistry, pharmacokinetics, behavioral effects, and clinical record, separating the verified record from the retracted, and provides sourcing, identity verification, reconstitution, and handling guidance for in vitro and in vivo investigative work.

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