SLU-PP-332 — Research Overview

Chemical Name: Not publicly disclosed as a systematic IUPAC name in all sources; designated SLU-PP-332 as a research compound identifier Molecular Weight: Approximately 290 Da (small organic molecule) Source: Developed at Saint Louis University (SLU) School of Medicine by Thomas Burris and colleagues; SLU-PP designates the Saint Louis University Pharmacology and Physiology program compound series Compound Class: Synthetic pan-agonist of estrogen-related receptors (ERRα, ERRβ, ERRγ) — a class of orphan nuclear receptor transcription factors. Important nomenclature clarification: SLU-PP-332 is a small synthetic organic molecule, not a peptide in the strict chemical definition. It is widely discussed in the peptide research community as an “exercise mimetic” compound due to its mechanism and application context, and is included in this catalog in that capacity. Receptor Targets and Potency: ERRα (EC50 = 98 nM, primary target), ERRβ (EC50 = 230 nM), ERRγ (EC50 = 430 nM) — measured in cell-based cotransfection/reporter assays. SLU-PP-332 was the first synthetic compound to achieve pharmacologically meaningful ERRα agonist potency, resolving a decades-long challenge in nuclear receptor pharmacology. Development of potent ERRα agonists had been hindered by the receptor’s constitutive activity and structural features that made agonist design difficult. Regulatory Status: Not FDA-approved. No clinical trials registered. Exclusively preclinical research stage as of this compilation. WADA Status: ERRα agonists and exercise mimetics are included on the WADA prohibited list under S4 (hormone and metabolic modulators). SLU-PP-332 has not been specifically named, but would likely fall under this category as an agent that activates metabolic pathways associated with exercise performance. Researchers using this compound in any sports context should be aware of this regulatory consideration. Key Publications: Billon et al., ACS Chemical Biology 2023 (primary pharmacology characterization; exercise mimetic activity); Xu et al., Circulation 2024 (heart failure application); Walker JK and Burris TP, Journal of Pharmacology and Experimental Therapeutics 2024 (metabolic syndrome); Frontiers in Physiology 2025 (aging muscle, human myoblast pilot data); multiple additional research group publications extending the ERR biology. Category: Orphan nuclear receptor (ERRα/β/γ) pan-agonist / synthetic exercise mimetic / mitochondrial biogenesis inducer / metabolic reprogramming tool / aerobic exercise gene program activator / preclinical research compound

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The scientific literature on this page is provided strictly for educational and informational purposes. All Rogue Compounds products are intended for in-vitro laboratory research use only and are not approved by the FDA for human or animal consumption. The studies referenced below are independent third-party peer-reviewed publications. Rogue Compounds makes no claims that any product diagnoses, treats, cures, or prevents any disease or condition. Researchers are responsible for compliance with all applicable local, state, and federal regulations.

What Is SLU-PP-332?

SLU-PP-332 is a synthetic small-molecule agonist of the estrogen-related receptor (ERR) family — three orphan nuclear receptors (ERRα, ERRβ, ERRγ) that function as master transcriptional regulators of cellular energy metabolism, mitochondrial biogenesis, and oxidative phosphorylation. Developed at Saint Louis University and first reported in peer-reviewed literature in 2022-2023, SLU-PP-332 represented a significant advance in nuclear receptor pharmacology: it was the first compound to demonstrate meaningful synthetic agonist activity at ERRα — a target that had resisted pharmacological activation for decades due to its constitutive high-activity state and challenging ligand-binding domain structure.

The biological significance of targeting the ERRs emerges from their role as transcriptional coordinators of the exercise adaptation response. When humans perform aerobic exercise, a coordinated transcriptional program activates in skeletal muscle and other metabolically active tissues — upregulating genes for mitochondrial biogenesis, oxidative phosphorylation, fatty acid oxidation, and oxygen delivery. ERRα sits at the regulatory apex of this program, driving the expression of hundreds of exercise-responsive genes in concert with its coactivator PGC-1α (peroxisome proliferator-activated receptor-gamma coactivator 1-alpha). Because ERRα orchestrates the transcriptional response to aerobic exercise at the gene level, pharmacological activation of ERRα constitutes a direct route to reproducing exercise adaptations without the mechanical work of exercise itself — which is the pharmacological concept of an exercise mimetic.

SLU-PP-332 is accurately described as the most pharmacologically validated synthetic ERRα agonist currently available as a research tool. Its ability to activate the aerobic exercise gene program in vitro and in vivo, improve exercise endurance in mice, enhance mitochondrial function across multiple organ systems, and improve metabolic parameters in obesity and metabolic syndrome models — all through the defined ERRα/ERRγ molecular mechanism — gives it a research profile that is mechanistically rigorous and biologically coherent even while remaining exclusively preclinical.

The ERR Nuclear Receptor Family — Biology and Pharmacological Context

The estrogen-related receptors were originally identified in 1988 based on their structural homology to the estrogen receptor (ER), but despite their name they do not bind estrogen or other steroid hormones — they are “orphan” nuclear receptors because no natural endogenous ligand has been identified. Their name reflects structural similarity to ER, not functional overlap. ERRα, ERRβ, and ERRγ share approximately 60-70% amino acid identity in their DNA-binding domains and ligand-binding domains.

The three ERR isoforms have distinct but overlapping expression patterns. ERRα is broadly expressed in metabolically active tissues — skeletal muscle, heart, kidney, brain, and adipose tissue — and is constitutively active, meaning it activates its target genes even without a ligand. ERRβ is expressed primarily in placenta, testis, and early development contexts. ERRγ is expressed in heart, brain, skeletal muscle, and other tissues and is the ERR isoform most highly expressed in cardiac tissue — where it plays a non-redundant role in regulating cardiac fatty acid metabolism. Both ERRα and ERRγ are essential for normal cardiac energy metabolism; mice lacking both ERRα and ERRγ in the heart develop severe cardiac failure.

ERRα’s constitutive activity was historically interpreted as meaning that agonist design was not possible — if the receptor is already active without a ligand, how would a synthetic agonist produce additional activation? The development of SLU-PP-332 resolved this apparent paradox by demonstrating that constitutive baseline activity does not preclude further pharmacological activation above that baseline. SLU-PP-332 increases ERRα transcriptional activity above its constitutive level — through a conformational change in the receptor’s activation helix (AF-2 helix) that enhances coactivator (PGC-1α) recruitment and downstream gene transcription. This pharmacological breakthrough opened ERRα to medicinal chemistry development that had previously been considered infeasible.

The Exercise Mimetic Concept — Scientific Foundation

The idea of a pharmacological exercise mimetic — a compound that produces the cellular adaptations of aerobic exercise without requiring the physical activity — has been discussed in the scientific literature since at least the early 2000s, following studies demonstrating that activating specific nuclear receptors (PPARδ, REV-ERBα) in mice could improve endurance capacity or alter muscle fiber composition. The practical appeal is substantial: for patients who cannot exercise (due to disability, severe cardiopulmonary disease, sarcopenia, musculoskeletal injury, or extreme obesity), exercise mimetics could provide metabolic benefits that physical exercise provides for healthy individuals.

Three types of exercise mimetics have been characterized in preclinical research:

PPARδ agonists (GW501516, also known as Cardarine): Act primarily through activation of fatty acid oxidation genes and produce endurance-enhancing effects in mice. GW501516 was abandoned during pharmaceutical development due to cancer-promoting effects discovered in long-term animal studies.

REV-ERBα agonists (SR-9011, SR-9009): Act through circadian clock pathway modulation and produce some metabolic and endurance benefits in animals. Their mechanism is distinct from both PPARδ and ERR pathways.

ERR agonists (SLU-PP-332 and related compounds): Act through the ERRα/PGC-1α axis to activate the aerobic exercise transcriptional program. This is the newest class, most mechanistically aligned with the acute exercise response, and — importantly — the class that does not carry the cancer-promoting signal that caused GW501516’s development halt. ERR agonists appear to activate a distinct set of exercise-responsive genes that does not overlap with the problematic oncogenic pathways activated by PPARδ agonists.

SLU-PP-332’s ERR-mediated mechanism is characterized as activating the “acute aerobic exercise program” — the immediate transcriptional response to a single bout of aerobic exercise — rather than the chronic training adaptation program. The key molecular signature of this acute program is induction of DDIT4 (DNA damage-inducible transcript 4, also called REDD1), which is rapidly and transiently elevated in skeletal muscle following aerobic exercise and serves as a master switch that directs downstream gene expression toward mitochondrial adaptation. SLU-PP-332 induces DDIT4 specifically through ERRα activation — a pharmacological recapitulation of the exercise-induced transcriptional cascade at its molecular origin.

Mechanism of Action

ERRα activation and PGC-1α coactivation — the master switch: SLU-PP-332 binds the ERRα ligand-binding domain and stabilizes the receptor in an active conformation that recruits PGC-1α as a coactivator. This ERRα-PGC-1α complex then drives transcription of hundreds of target genes by binding estrogen-related receptor response elements (ERREs) in their promoters. The ERRα/PGC-1α axis is the primary transcriptional coordinator of mitochondrial biogenesis — new mitochondria synthesis — in skeletal muscle and cardiac tissue. This is the same axis activated by endurance exercise training.

DDIT4-mediated acute exercise gene program: The most highly upregulated gene in SLU-PP-332-treated skeletal muscle is DDIT4 — the protein identified as a key initiator of the acute aerobic exercise transcriptional response. DDIT4 knockout mice exhibit severely impaired mitochondrial respiration in skeletal muscle and reduced exercise capacity. SLU-PP-332’s induction of DDIT4 specifically requires ERRα (it is abolished in ERRα-knockout mice), establishing the mechanistic chain: SLU-PP-332 → ERRα activation → DDIT4 induction → acute exercise transcriptional program → downstream mitochondrial and metabolic adaptations.

Mitochondrial biogenesis and oxidative capacity: Downstream of DDIT4 and the ERRα/PGC-1α cascade, SLU-PP-332 drives transcriptional upregulation of genes encoding mitochondrial respiratory chain components, fatty acid oxidation enzymes, and proteins required for oxidative phosphorylation. In C2C12 skeletal muscle cells, SLU-PP-332 treatment for 24 hours produced measurable increases in maximum mitochondrial respiration and substantial increases in mitochondrial biogenesis (assessed by MitoTracker staining). In vivo, repeated SLU-PP-332 administration produced a shift in skeletal muscle fiber type toward type IIa oxidative fibers (fast-twitch oxidative fibers that use oxidative phosphorylation for ATP generation rather than glycolysis) — the same fiber type shift produced by aerobic endurance training.

Fatty acid oxidation — the fuel substrate shift: Aerobic exercise training shifts skeletal muscle and cardiac metabolism toward preferential use of fatty acids as fuel — the metabolic flexibility associated with endurance fitness. SLU-PP-332 activates fatty acid oxidation genes in both skeletal muscle and cardiac tissue, increasing the uptake and catabolism of free fatty acids for ATP production and reducing dependence on glucose. In obese mice, this shift to fatty acid oxidation is directly linked to fat mass reduction without reduced food intake.

Cardiac-specific mechanism — ERRγ dependence: While skeletal muscle effects are primarily ERRα-dependent, the cardiac benefits of SLU-PP-332 operate primarily through ERRγ. Genetic studies using siRNA knockdown in cardiac cells established that ERRγ — not ERRα or ERRβ — mediates most of the transcriptional activation of metabolic genes in cardiomyocytes by SLU-PP-332. ERRγ knockdown abolished the metabolic gene transcription induced by SLU-PP-332 in cardiomyocytes. This isoform-specific cardiac mechanism distinguishes SLU-PP-332’s cardiac pharmacology from its skeletal muscle pharmacology and is mechanistically significant for the heart failure application.

E2F1 pathway modulation in cardiac tissue: RNA sequencing of SLU-PP-332-treated cardiomyocytes identified downregulation of cell cycle genes as a secondary transcriptional effect, partially mediated through E2F1 — a transcription factor involved in cell cycle progression. This cell cycle gene suppression in the context of heart failure is potentially beneficial, as cardiomyocyte proliferative responses are associated with pathological hypertrophic remodeling. SLU-PP-332 improved ejection fraction and reduced fibrosis without affecting cardiac hypertrophy — a profile consistent with metabolic benefit without the pathological structural changes that would worsen heart failure outcomes.

Published Research

Study 1 — Primary Pharmacological Characterization and Exercise Mimetic Activity

Authors: Billon C, Murray MH, Bhatt DL, Kolber MA, Kliewer SA, Mangelsdorf DJ, Burris TP et al. (Saint Louis University) Year: 2023 Journal: ACS Chemical Biology Reference: ACS Chem Biol 2023;18:756-768 (and bioRxiv preprint 2022) Full text: https://pmc.ncbi.nlm.nih.gov/articles/PMC11584170/

This paper was the primary published characterization of SLU-PP-332 as a pharmacological tool and exercise mimetic — establishing both the molecular pharmacology and the in vivo exercise endurance effects.

SLU-PP-332 was characterized as a pan-ERR agonist with highest potency at ERRα (EC50 = 98 nM), followed by ERRβ (230 nM) and ERRγ (430 nM) in cotransfection/reporter assays. A well-characterized ERR target gene, PDK4 (pyruvate dehydrogenase kinase 4), was induced by SLU-PP-332 in skeletal muscle cells — establishing ERR target gene activation in a physiologically relevant cell context.

In C2C12 skeletal muscle cells, 24-hour SLU-PP-332 treatment increased maximum mitochondrial respiration and induced substantial mitochondrial biogenesis by MitoTracker staining. These in vitro findings demonstrated ERR-dependent metabolic reprogramming in a skeletal muscle model before proceeding to in vivo studies.

In vivo administration to mice induced DDIT4 — the key acute exercise transcriptional initiator — specifically through ERRα. In conditional ERRα knockout mice (mERRα−/−), DDIT4 induction was abolished, directly establishing ERRα as the essential receptor mediating SLU-PP-332’s exercise gene program.

Treadmill endurance testing in SLU-PP-332-treated versus vehicle-treated mice demonstrated significant improvements in exercise endurance — treated mice ran approximately 70% longer and 45% further than controls, with increased proportions of type IIa oxidative muscle fibers in histological analysis.

These findings established the proof-of-concept: pharmacological ERRα activation reproduces the exercise endurance enhancement and muscle fiber type shift associated with aerobic training through the defined DDIT4-mediated exercise gene program.

Study 2 — Metabolic Syndrome Application: Obesity and Insulin Resistance

Authors: Walker JK, Burris TP et al. (Saint Louis University) Year: 2024 Journal: Journal of Pharmacology and Experimental Therapeutics

This study directly evaluated SLU-PP-332 in preclinical models of obesity and metabolic syndrome — the primary proposed therapeutic application — using both diet-induced obese (DIO) mice and the genetically obese ob/ob mouse model.

Diet-induced obese mice and ob/ob mice received SLU-PP-332 at 50 mg/kg intraperitoneally twice daily for 28 days (DIO) or 12 days (ob/ob). SLU-PP-332 increased resting energy expenditure — mice burned more calories at rest — without significant changes in food intake.

Fatty acid oxidation increased substantially — a 25% increase in fatty acid oxidation was documented, consistent with the ERRα-driven shift to oxidative fatty acid metabolism rather than glucose oxidation.

Fat mass decreased by approximately 12% over 28 days in DIO mice — a meaningful reduction in adiposity driven by increased metabolic expenditure and fatty acid oxidation without caloric restriction.

Glucose tolerance improved and insulin sensitivity markers were restored — demonstrating that the metabolic reprogramming from ERRα activation produces clinically relevant improvements in the insulin resistance and glucose dysregulation that characterize metabolic syndrome.

Gene expression analysis in skeletal muscle, liver, and adipose tissue confirmed activation of ERR target genes involved in fatty acid oxidation and mitochondrial metabolism — establishing that the gene-level effects translate to whole-body metabolic outcomes.

Study 3 — Heart Failure Application: Cardiac Metabolism and Function

Authors: Xu W, Zhang L, Billon C, Burris TP et al. (Baylor College of Medicine) Year: 2024 Journal: Circulation Reference: Circulation 2024;149(3):227-250 DOI: 10.1161/CIRCULATIONAHA.123.066542

This Circulation paper was the largest and most clinically significant study of SLU-PP-332 to date, demonstrating cardioprotective effects in a pressure overload-induced heart failure model — a standard and clinically validated preclinical model of cardiac failure.

Mice underwent transaortic constriction (TAC) surgery to induce chronic pressure overload cardiac failure, then received SLU-PP-332 or a structurally distinct pan-ERR agonist (SLU-PP-915) for 6 weeks. Both compounds significantly improved ejection fraction, reduced cardiac fibrosis, and increased survival associated with pressure overload-induced heart failure — without affecting cardiac hypertrophy (the maladaptive structural enlargement that worsens heart failure outcomes).

Multi-omics analysis (RNA sequencing and metabolomics) comprehensively characterized the mechanism: ERR agonists transcriptionally activated a broad spectrum of metabolic genes, particularly genes in fatty acid metabolism and oxidative phosphorylation pathways — restoring the cardiac metabolic gene program that is suppressed in failing hearts. Metabolomics confirmed normalization of metabolic profiles in fatty acid/lipid and TCA/OXPHOS metabolite pathways.

Genetic isoform-dependency studies established that ERRγ — not ERRα or ERRβ — was the primary mediator of the cardiac transcriptional and functional effects. siRNA knockdown of ERRγ abolished most ERR agonist-induced metabolic gene transcription in cardiomyocytes, while ERRα or ERRβ knockdown had substantially lesser effects.

The biological rationale for these findings is mechanistically clear: the failing heart undergoes a “metabolic shift” away from fatty acid oxidation (the primary fuel for normal cardiac energy production) toward glucose metabolism. This metabolic remodeling is initially compensatory but ultimately maladaptive — cardiac ATP production falls progressively. ERRγ agonism with SLU-PP-332 restores the fatty acid oxidation gene program, reverting the failing heart’s metabolism toward the normal cardiac fuel preference and improving contractile function.

This study also had broader pharmacological significance: by demonstrating that two structurally distinct pan-ERR agonists (SLU-PP-332 and SLU-PP-915) both produced cardiac benefit through the same mechanism, it established that the cardioprotective effect is an on-target ERR agonist class effect rather than a compound-specific property.

Study 4 — Aging Kidney: Mitochondrial Dysfunction and Inflammation Reversal

Authors: Wang X et al. (and independent group) Year: 2023 Journal: American Journal of Pathology

This study extended SLU-PP-332’s application to aging-related organ pathology in the kidney — the third organ system (alongside skeletal muscle and heart) demonstrating ERR agonist benefit in distinct tissue-specific contexts.

Age-related kidney dysfunction is characterized by progressive mitochondrial dysfunction, oxidative stress, and chronic low-grade inflammation in renal tubular cells — the tubular cells that perform the kidney’s metabolic filtration work and are highly dependent on mitochondrial oxidative phosphorylation for ATP. ERR agonism with SLU-PP-332 reversed these aging-associated changes.

Restored renal mitochondrial respiration by approximately 60% in aged rodent models — a magnitude of restoration comparable to effects observed with endurance exercise training in other organ systems.

Reduced age-associated inflammatory markers (IL-6, TNF-alpha) in renal tissue, demonstrating that mitochondrial restoration attenuates the chronic inflammatory state associated with mitochondrial dysfunction in aging kidney.

Anti-fibrotic effects were observed — reducing the progressive fibrosis that characterizes age-related kidney disease and contributes to declining renal function — consistent with the connection between mitochondrial dysfunction, oxidative stress, and TGF-beta-mediated fibrotic signaling in aging kidney.

These renal findings expanded the proposed therapeutic applications of ERR agonism from metabolic and cardiovascular contexts into the realm of age-related nephropathy — a condition with limited treatment options and substantial global disease burden.

Study 5 — Human Myoblast Pilot Data: Aging Muscle from Inactive Adults

Authors: Multiple Italian investigators Year: 2025 Journal: Frontiers in Physiology

This pilot study introduced a human biological element to SLU-PP-332 research — evaluating its effects on primary myoblast cultures derived from muscle biopsies of inactive versus active adult women undergoing hip arthroplasty.

Twenty women were classified as active (meeting physical activity guidelines) or inactive (not meeting guidelines) based on self-reported activity. Muscle biopsies were taken during surgery and primary myoblast cultures established. Inactive group myoblasts were treated with SLU-PP-332.

SLU-PP-332 treatment of inactive myoblasts produced upregulation of SIRT1, PGC-1α, and ERRα — the key regulators of mitochondrial biogenesis — to levels comparable to those observed in untreated cells from the active group. This direct comparison established that SLU-PP-332 pharmacologically restored the exercise-associated molecular signature in human muscle cells from sedentary individuals.

Markers of cellular senescence (SA-beta-galactosidase), oxidative stress (ROS production), and cellular damage (LDH release) were reduced by SLU-PP-332 treatment in inactive myoblasts — while glutathione (an endogenous antioxidant) increased.

Myotube formation — the process by which myoblasts fuse into functional muscle fibers — was improved in SLU-PP-332-treated inactive cells, with MyHC (myosin heavy chain, a marker of differentiated muscle fiber) expression restored toward active group levels. Akt (a pro-survival/anabolic signaling kinase) and Bcl-2 (an anti-apoptotic protein) expression both improved with treatment — consistent with reduced sarcopenia-associated apoptosis in treated muscle cells.

This study is the first to use human-derived biological material to evaluate SLU-PP-332’s effects. Its design — comparing drug-treated human sedentary myoblasts to untreated active myoblasts — provides a preliminary human biological validation that the ERR agonist mechanism produces effects in human muscle cells qualitatively comparable to those from physical activity. It is not a clinical trial and does not constitute evidence of human therapeutic efficacy, but it represents an important step toward biological plausibility in human tissue.

SLU-PP-332 and the Exercise Mimetic Landscape — Comparison to GW501516

Because SLU-PP-332 is discussed in the exercise mimetic context, its comparison to GW501516 (Cardarine) — the most widely known prior exercise mimetic research compound — is essential for accurate research contextualization.

GW501516 is a PPARδ agonist that was abandoned in pharmaceutical development following the discovery that long-term administration produced dose-dependent rapid tumor development across multiple tissue types in long-term animal carcinogenicity studies. This oncogenic signal was considered definitive by regulatory agencies, and further clinical development was halted.

SLU-PP-332 acts through a pharmacologically distinct mechanism — ERRα/ERRγ activation rather than PPARδ. These receptors regulate overlapping but distinct transcriptional programs. The exercise gene signature activated by ERR agonists (DDIT4-mediated acute exercise program) is different from the fatty acid oxidation program activated by PPARδ. No long-term carcinogenicity data exist for SLU-PP-332 in any species. ERRα is expressed in breast and other cancer cell lines and has been studied in cancer biology — the implication of ERRα agonism for cancer risk is an acknowledged unknown that requires characterization before any human therapeutic application can be responsibly considered.

This comparison is not intended to predict that SLU-PP-332 will share GW501516’s safety problems — there is no evidence of this. It is intended to establish that the absence of evidence of harm is not the same as evidence of absence of harm, particularly for a compound with no human safety data and a target receptor implicated in cancer cell biology.

Honest Assessment — What the Evidence Shows and What It Does Not

What the evidence clearly shows: SLU-PP-332 is a potent ERRα agonist that pharmacologically activates the acute aerobic exercise transcriptional program in skeletal muscle through a defined ERRα-DDIT4 mechanism. This produces measurable improvements in exercise endurance, mitochondrial function, oxidative fiber composition, energy expenditure, fatty acid oxidation, and fat mass reduction in mouse models. Additional independently published studies demonstrate cardiac benefit in heart failure models (through ERRγ) and renal benefit in aging models. Human myoblast pilot data provide preliminary biological plausibility in human tissue.

What the evidence does not show: No human safety data of any kind. No pharmacokinetic data in humans. No long-term toxicology in any species. No evidence regarding the oncological safety of chronic ERRα agonism in human tissue. No dose translation framework from mice to humans — preclinical doses (50 mg/kg twice daily in mice) do not translate directly to human doses by simple body weight scaling. No clinical trial registration in any jurisdiction.

The research community using SLU-PP-332 as an in vitro or in vivo preclinical tool is on solid scientific ground — the compound has been extensively characterized and validated as a research instrument for studying ERR-dependent transcriptional programs. The broader longevity and performance research community that has adopted SLU-PP-332 for human application is outpacing the evidence base — which remains entirely preclinical — by a significant margin.

Current Research Status

SLU-PP-332 research is advancing rapidly in academic settings. Multiple independent research groups have published on the compound across skeletal muscle, cardiac, metabolic, and renal biology since its initial report. The Saint Louis University group continues to develop structurally distinct pan-ERR agonists (including SLU-PP-915 and related analogs) with improved pharmacokinetic properties for potential therapeutic development. Long-term toxicology studies and cancer safety evaluation are essential prerequisites for clinical development that have not yet been publicly reported. No Phase 1 trial has been registered or initiated as of this compilation.

Available from Rogue Compounds

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