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superstack

shredding superstack

ten compounds aimed at fat loss: less eaten, more fat released, more of it burned as heat

  1. SANA
    creatine-driven heat production in fat
    Early human trials
  2. ATX-304
    AMPK activator, mild mitochondrial uncoupler
    Early human trials
  3. BAM15
    the mitochondrial uncoupler
    Preclinical
  4. SLU-PP-915
    the oral ERR agonist
    Preclinical
  5. 5-Amino-1MQ
    the NNMT inhibitor
    Preclinical
  6. Mirabegron
    β3 agonist
    Early human trials
  7. MOTS-c
    mitochondrial peptide
    Preclinical
  8. ITPP
    oxygen-release agent
    Preclinical
  9. botanical extract
    Somatropin (HGH)
    growth hormone itself
    Established
  10. Tirzepatide
    GIP and GLP-1 agonist; the one that cuts intake
    Established

Protocol

as reported; not a recommendation
CompoundRouteDose rangeTiming
SANAOral200–400 mg/daySplit AM/PM
ATX-304 SodiumOral200–400 mg/daySplit AM/PM
BAM15Oral200–400 mg/daySplit AM/PM
SLU-PP-915Oral20–50 mg/daySplit AM/PM or Pre Cardio
5-Amino-1MQOral100–200 mg/daySplit AM/PM
MirabegronOral100–200 mg/daySplit AM/PM
MOTS-cSubQ10–15 mg/weekSplit 3x Weekly
ITPPSubQ100–225 mg/weekSplit 3x Weekly
HGHSubQ2–4 IU/dayPre Bed
TirzepatideSubQ2.5–15 mg (user dependent)Weekly

What everything does

CompoundWhat it does
SANABinds the mitochondrial creatine kinases CKMT1/2 [1] and raises creatine-dependent heat production in fat tissue, without UCP1 and independently of AMPK [2].
ATX-304 SodiumActivates AMPK across its isoforms [3]. Also a mild mitochondrial uncoupler, which lets muscle take up and burn glucose independently of insulin [4].
BAM15Carries protons across the inner mitochondrial membrane, bypassing ATP synthase, so fuel is burned without making ATP [5].
SLU-PP-915Activates the ERRα, ERRβ and ERRγ nuclear receptors [6], switching on mitochondrial-biogenesis and fuel-selection genes [7] and the gene programme of aerobic exercise [8].
5-Amino-1MQInhibits the enzyme NNMT [9], which raises NAD+ and SAM in fat cells and suppresses fat synthesis [10].
MirabegronActivates β3 adrenergic receptors, stimulating lipolysis in white fat [11], and raises brown-fat activity and resting energy expenditure [12].
MOTS-cInhibits the folate cycle in skeletal muscle, which activates AMPK and raises the glucose transporter GLUT4 [13].
ITPPEnters red blood cells and lowers haemoglobin's affinity for oxygen, so more oxygen is released to tissue [14].
HGHActivates the growth hormone receptor and raises IGF-1 [15]. Raises circulating free fatty acids and glycerol [16], lowers fat mass and raises lean mass [17].
TirzepatideActivates the GIP and GLP-1 receptors [18], lowering appetite and food intake [19].

Why it works

Appetite suppression

Tirzepatide is the one compound here that acts on energy intake. Activating the GIP and GLP-1 receptors lowers appetite and food intake [19] and slows stomach emptying, most strongly after the first dose [20].

Lipolysis

Stored fat leaves fat cells as free fatty acids by two routes. Mirabegron stimulates lipolysis in white fat through β3 receptors [11]. Growth hormone raises circulating free fatty acids and glycerol [16].

Fat oxidation

Four compounds push cells towards oxidising fat. Three do it through AMPK, the cell's energy-shortage sensor: ATX-304 activates it directly [3], MOTS-c through the folate cycle [13], and BAM15 as a consequence of uncoupling [21]. SLU-PP-915 works through the ERR nuclear receptors, which raise mitochondrial oxidative capacity and fatty acid use in heart muscle [22].

Thermogenesis

Four compounds burn fuel as heat, each by a different mechanism. BAM15 leaks protons across the inner mitochondrial membrane, so respiration runs without making ATP [5], and ATX-304 is a milder uncoupler [4]. SANA drives creatine-dependent heat production in fat tissue without UCP1 [2]. Mirabegron activates brown fat and raises resting energy expenditure [12], and raises UCP1 and other beige-fat markers in subcutaneous fat [23].

Oxygen delivery

Burning fuel as heat uses oxygen. BAM15 raises mitochondrial respiration [5], ATX-304 raised basal oxygen consumption in kidney cells [24] and SANA raises respiration in fat tissue [2]. ITPP works on the supply side: it shifts haemoglobin towards releasing its oxygen, so more reaches tissue where oxygen is low [14].

Lipogenesis inhibition

5-Amino-1MQ inhibits NNMT, which raises NAD+ and SAM in fat cells and suppresses the synthesis of new fat [10]. ATX-304 shifts the liver away from lipid synthesis and towards fatty acid oxidation [25].

Insulin sensitivity

ATX-304 raises glucose uptake in muscle independently of insulin [4], and MOTS-c raises the glucose transporter GLUT4 in skeletal muscle [13]. Tirzepatide [26] and mirabegron [27] improve insulin sensitivity. BAM15 [28] and SANA [1] lowered insulin resistance in obese mice.

Exercise capacity

SLU-PP-915 raises the mitochondrial-biogenesis gene PGC1α [7], switches on the gene programme of aerobic exercise and raised running endurance in mice [8], as did MOTS-c [29]. ITPP, which raises oxygen delivery, also raised exercise capacity in mice [30].

Lean mass preservation

Growth hormone raises IGF-1, which mediates most of its anabolic effects [15], and raises lean body mass while fat mass falls [17]. BAM15 lowered fat mass in obese mice without loss of lean mass [28] and activated mitophagy, the mitochondrial quality-control pathway, in muscle [31].

References

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    PAN-AMPK activator O304 improves glucose homeostasis and microvascular perfusion in mice and type 2 diabetes patients.
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    Tirzepatide is an imbalanced and biased dual GIP and GLP-1 receptor agonist.
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Not a recommendation to take or combine anything. Doses are reported, not prescribed. Read the individual entries, and talk to a clinician before taking any of this, particularly anything labelled prescription drug.