≥99% Purity — HPLC + Mass Spec ◆ For Laboratory Research Use Only
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Adipotide FTPP (2mg & 5mg)

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A dual-function prohibitin-targeting proapoptotic peptide (FTPP) that selectively destroys white adipose vasculature. Produced dramatic fat loss in primate studies but clinical development was discontinued due to dose-dependent renal toxicity. HPLC-MS verified >99% purity, CAS 859216-15-2.

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SKU: ADIPOTIDE-2-5mgCategory: Peptides

Adipotide FTPP (10mg): The Prostate-Homing Peptide-Conjugated Apoptosis-Inducing Peptide — A Targeted Anti-Adiposity Research Compound That Selectively Destroys White Adipose Tissue Vasculature to Produce Rapid Fat Loss, Improved Insulin Sensitivity, and Metabolic Benefits in Preclinical Obesity Research

Adipotide (also known as FTPP, CKGGRAKDC-GG-D(KLAKLAK)2, or prostate-homing peptide [PHP]-conjugated pro-apoptotic peptide) is a chimeric peptide consisting of two functional domains: (1) a targeting domain — the prostate-homing peptide (PHP, CKGGRAKDC), which was originally identified as a peptide that homes to prostate tumor vasculature but was subsequently found to also bind to white adipose tissue (WAT) vasculature (specifically to prohibitin [PHB], a protein expressed on the surface of endothelial cells in white adipose tissue blood vessels and prostate tumor blood vessels, but not on normal tissue vasculature); and (2) an apoptosis-inducing (pro-apoptotic) domain — the D(KLAKLAK)2 peptide, a cationic, amphipathic α-helical antimicrobial peptide (also known as "KLAK" or "mitochondrial pro-apoptotic peptide") that disrupts mitochondrial membranes, triggering the intrinsic (mitochondrial) apoptosis pathway (cytochrome c release, caspase-9/caspase-3 activation, DNA fragmentation, cell death). The two domains are connected by a glycine-glycine (GG) linker that provides flexibility between the targeting and effector domains. The mechanism of action is: (1) Adipotide is administered systemically (subcutaneous or intravenous injection); (2) the PHP targeting domain binds to prohibitin (PHB) on the surface of endothelial cells lining the blood vessels of white adipose tissue (and prostate tumors); (3) the peptide is internalized into the endothelial cell via receptor-mediated endocytosis; (4) the pro-apoptotic KLAK domain is released (or acts within the endosome/mitochondria) and disrupts mitochondrial membranes, triggering apoptosis (programmed cell death) of the adipose tissue endothelial cell; (5) destruction of the adipose tissue vasculature cuts off blood supply to the white adipocytes, causing them to undergo secondary apoptosis/necrosis (similar to how anti-angiogenic therapies starve tumors); (6) the dead adipocytes and endothelial cells are cleared by macrophages and the immune system, resulting in reduced white adipose tissue mass (fat loss); (7) the reduced fat mass leads to improved metabolic parameters: decreased body weight, improved insulin sensitivity, decreased fasting glucose and insulin, improved lipid profile, decreased hepatic steatosis. Adipotide was developed by researchers at the MD Anderson Cancer Center (originally as a prostate cancer therapy — the PHP domain homes to prostate tumor vasculature, and the KLAK domain kills the tumor endothelial cells, starving the prostate tumor). However, researchers serendipitously discovered that Adipotide also caused dramatic fat loss in treated animals (because PHB is also expressed on white adipose tissue vasculature), leading to its investigation as an anti-obesity therapy. Preclinical studies in rhesus monkeys (a highly relevant primate model) demonstrated: (1) significant dose-dependent weight loss (~10-15% body weight reduction over 4 weeks of treatment); (2) reduced body mass index (BMI) and waist circumference; (3) improved insulin sensitivity (decreased fasting insulin, decreased HOMA-IR, improved glucose tolerance); (4) decreased subcutaneous and visceral fat mass (measured by DEXA and MRI); (5) the weight loss was primarily fat mass (lean mass was relatively preserved); (6) the effects were reversible (weight gradually returned after treatment cessation, as adipose tissue vasculature regenerated); (7) generally well-tolerated at therapeutic doses (some mild renal toxicity at higher doses — the peptide is cleared by the kidneys and can cause mild tubular injury at high doses). Adipotide represents a completely novel and radical approach to obesity treatment — unlike current therapies (GLP-1 agonists, etc.) which work by reducing appetite and increasing satiety (acting on the central nervous system), Adipotide works by physically destroying white adipose tissue vasculature, causing direct fat mass reduction. This "anti-angiogenic" approach to fat loss is conceptually similar to how anti-angiogenic cancer therapies (e.g., bevacizumab/Avastin) work by cutting off tumor blood supply. However, Adipotide development was ultimately discontinued (partly due to safety concerns — renal toxicity at higher doses, and the theoretical concern that destroying adipose tissue vasculature could have systemic effects; partly due to the success and commercial dominance of GLP-1 agonists which have a more favorable safety profile; and partly due to business/strategic decisions). Adipotide remains a valuable research tool for studying: adipose tissue biology, angiogenesis in fat tissue, prohibitin (PHB) as a therapeutic target, targeted peptide drug delivery, pro-apoptotic peptide therapeutics, and novel approaches to obesity treatment. The research-grade Adipotide supplied by Amideworks is intended for laboratory and investigational use only, not for human consumption or therapeutic use[1][2][3][4][5][6][7][8][9][10].

Adipotide Mechanism of Action: Targeted Destruction of White Adipose Tissue Vasculature

Adipotide (FTPP): Targeted White Adipose Tissue Vasculature Destruction 1. Systemic Circulation PHP KLAK Adipotide = PHP (targeting) + GG linker + KLAK (apoptosis) SC or IV injection 2. Targeting & Binding WAT Blood Vessel (endothelium) PHB receptors PHP PHP domain binds to prohibitin (PHB) on WAT endothelial cells Specific: not normal tissue vasculature 3. Internalization & Apoptosis Endothelial Cell Mito KLAK disrupts mitochondrial membranes → caspase apoptosis 4. Vasculature Destroyed Destroyed WAT Vasculature ✕ ✕ ✕ Blood supply to adipocytes cut off Adipocytes starve → secondary death Macrophages clear dead tissue 5. Fat Loss & Metabolic Benefits Fat Before Lean After ↓ Body weight (~10-15%) ↓ Insulin resistance

Key Research Applications for Adipotide

Research Highlight: Adipotide (FTPP) produced dramatic, dose-dependent weight loss in rhesus monkeys (a highly relevant primate model) — ~10-15% body weight reduction over just 4 weeks of treatment, with the weight loss being primarily fat mass (lean mass preserved). This is a completely novel mechanism of fat loss: unlike GLP-1 agonists which work by reducing appetite (CNS-mediated), Adipotide physically destroys white adipose tissue vasculature, cutting off blood supply to fat cells and causing them to die. This "anti-angiogenic" approach to obesity is conceptually revolutionary but was ultimately discontinued due to safety concerns (renal toxicity at higher doses) and the commercial success of GLP-1 agonists.
  • Obesity and Weight Loss Research (Novel Anti-Angiogenic Approach): Adipotide is primarily investigated for obesity and weight loss through a completely novel mechanism — targeted destruction of white adipose tissue (WAT) vasculature. Unlike current obesity therapies (GLP-1 agonists, etc.) which work by reducing appetite and increasing satiety (acting on the central nervous system/hypothalamus), Adipotide works peripherally by physically destroying the blood vessels that supply white fat tissue, causing the fat cells to die from lack of blood supply (similar to how anti-angiogenic cancer therapies starve tumors). Preclinical studies in rhesus monkeys demonstrated: (a) significant dose-dependent weight loss (~10-15% body weight reduction over 4 weeks); (b) reduced BMI and waist circumference; (c) decreased subcutaneous and visceral fat mass (measured by DEXA and MRI); (d) the weight loss was primarily fat mass (lean mass was relatively preserved — an important advantage over simple caloric restriction which often causes muscle loss); (e) the effects were reversible (weight gradually returned after treatment cessation as adipose tissue vasculature regenerated — this is both a limitation [not a permanent cure] and a safety feature [effects are reversible]); (f) rapid onset of action (significant weight loss within 1-2 weeks, faster than GLP-1 agonists which typically take 4-8 weeks for significant weight loss). Research-grade Adipotide is used to study: adipose tissue angiogenesis, the role of vasculature in fat mass maintenance, prohibitin (PHB) as a target for obesity, targeted peptide therapeutics for metabolic disease, and comparison with other weight loss mechanisms (appetite suppression, increased energy expenditure, lipolysis, malabsorption)[1][2][3][4].
  • Insulin Sensitivity and Type 2 Diabetes Research: Beyond weight loss, Adipotide has significant effects on insulin sensitivity and glucose homeostasis. The reduction in white adipose tissue mass (particularly visceral fat, which is strongly associated with insulin resistance) leads to: (a) decreased fasting insulin levels; (b) decreased HOMA-IR (homeostatic model assessment of insulin resistance); (c) improved glucose tolerance (improved oral glucose tolerance test [OGTT] results); (d) decreased fasting glucose (in diabetic/obese animal models); (e) improved insulin signaling in peripheral tissues (increased Akt phosphorylation in muscle and liver); (f) decreased adipose tissue inflammation (reduced M1 macrophage infiltration, reduced pro-inflammatory cytokines [TNF-α, IL-6, MCP-1] — adipose tissue inflammation is a key driver of insulin resistance); (g) decreased ectopic fat deposition in liver and muscle (lipotoxicity is another key driver of insulin resistance). In rhesus monkey studies, Adipotide improved insulin sensitivity independently of (or in addition to) its weight loss effects — some metabolic improvements were observed before significant weight loss occurred, suggesting that Adipotide may have direct metabolic benefits beyond simple fat reduction (possibly through reduced adipose tissue inflammation and improved adipokine profile [increased adiponectin, decreased leptin]). Research-grade Adipotide is used to study: the relationship between adipose tissue vasculature and insulin sensitivity, the role of visceral fat in metabolic disease, novel insulin-sensitizing mechanisms, and comparison with other insulin-sensitizing therapies (metformin, thiazolidinediones, GLP-1 agonists)[1][2][5].
  • Prostate Cancer Research (Original Indication): Adipotide was ORIGINALLY developed as a prostate cancer therapy, not an obesity therapy. The prostate-homing peptide (PHP, CKGGRAKDC) was identified through in vivo phage display screening as a peptide that specifically homes to prostate tumor vasculature (binding to prohibitin [PHB] which is expressed on prostate tumor endothelial cells but not normal endothelium). The KLAK pro-apoptotic domain was added to kill the tumor endothelial cells, cutting off blood supply to the prostate tumor (an anti-angiogenic cancer therapy approach). In preclinical prostate cancer models, Adipotide demonstrated: (a) specific homing to prostate tumor vasculature (not normal tissue); (b) destruction of prostate tumor blood vessels; (c) reduced prostate tumor growth and tumor volume; (d) increased tumor cell apoptosis; (e) reduced tumor angiogenesis. The fat loss was a SERENDIPITOUS discovery — researchers noticed that animals treated with Adipotide for prostate cancer also lost significant amounts of fat, which led to the realization that PHB is also expressed on white adipose tissue vasculature (not just prostate tumor vasculature), and that Adipotide destroys both prostate tumor and white fat vasculature. Research-grade Adipotide is still used to study: prostate tumor angiogenesis, prohibitin (PHB) as a cancer target, targeted peptide drug delivery to tumors, anti-angiogenic cancer therapies, and the relationship between tumor and adipose tissue vasculature (both express PHB, suggesting a shared angiogenic phenotype)[3][6][7].
  • Targeted Peptide Drug Delivery and Pro-Apoptotic Peptide Research: Adipotide is a valuable research tool for studying targeted peptide drug delivery and pro-apoptotic peptide therapeutics. Its design represents a classic "magic bullet" approach: (a) a targeting domain (PHP) that specifically binds to a cell-surface marker (PHB) on the target cell type (WAT endothelial cells, prostate tumor endothelial cells); (b) a flexible linker (GG) that connects the targeting and effector domains while maintaining their independent folding/function; (c) an effector domain (KLAK) that induces cell death once internalized into the target cell. This modular design is widely used in targeted therapeutics (antibody-drug conjugates [ADCs], peptide-drug conjugates, targeted toxins, etc.). Research-grade Adipotide is used to study: (a) peptide-based targeting moieties (how to identify and optimize homing peptides through phage display); (b) prohibitin (PHB) as a cell-surface target for drug delivery (PHB is expressed on WAT and tumor vasculature but not normal endothelium, making it a useful target); (c) pro-apoptotic peptides (KLAK and related cationic amphipathic α-helical peptides that disrupt mitochondrial membranes); (d) linker design (how to optimize the linker between targeting and effector domains for stability, flexibility, and cleavage); (e) receptor-mediated endocytosis (how targeted peptides are internalized into cells); (f) endosomal escape (how pro-apoptotic peptides escape from endosomes to reach mitochondria); (g) pharmacokinetics and biodistribution of targeted peptides (how to optimize half-life, tissue distribution, and clearance); (h) immunogenicity of peptide therapeutics (how to minimize antibody formation against therapeutic peptides)[3][6][8].
  • Adipose Tissue Biology and Angiogenesis Research (Basic Science): Adipotide is a valuable tool for studying the basic biology of white adipose tissue, particularly the role of angiogenesis (blood vessel formation) in fat tissue growth and maintenance. Key research areas include: (a) the relationship between adipose tissue vasculature and fat mass (Adipotide demonstrates that destroying WAT vasculature causes fat loss, proving that adipose tissue is dependent on its blood supply like any other tissue); (b) the "angiogenic switch" in adipose tissue (how fat tissue recruits blood vessels during weight gain, and how inhibiting angiogenesis can prevent fat growth); (c) prohibitin (PHB) expression and function in adipose tissue endothelial cells (why PHB is expressed on WAT endothelium but not normal endothelium — possibly related to the active angiogenic state of expanding fat tissue); (d) the role of endothelial cells in adipose tissue homeostasis (endothelial cells are not just passive conduits — they actively regulate adipocyte function, inflammation, and metabolism through paracrine signaling); (e) adipose tissue remodeling after vasculature destruction (how dead adipocytes are cleared by macrophages, how fibrosis develops, how the tissue regenerates after treatment cessation); (f) the difference between subcutaneous and visceral adipose tissue vasculature (do they have different PHB expression levels? Does Adipotide preferentially destroy one type over the other?); (g) brown adipose tissue (BAT) vs. white adipose tissue (WAT) vasculature (does Adipotide affect BAT? BAT has a much denser vasculature and different endothelial phenotype — if Adipotide spares BAT, that would be beneficial since BAT is metabolically active and beneficial); (h) the role of adipose tissue vasculature in insulin resistance and metabolic inflammation (endothelial dysfunction in fat tissue is an early event in obesity-related metabolic disease). Research-grade Adipotide is used alongside other tools (VEGF inhibitors, angiopoietin inhibitors, genetic models of adipose angiogenesis) to map the complex relationship between fat tissue vasculature and metabolic health[4][5][9][10].

References

  1. Kolonin MG, Saha PK, Chan L, et al. Reversal of obesity by targeted ablation of adipose tissue. Nat Med. 2004;10(6):625-632. (Landmark paper — the original discovery that targeted ablation of white adipose tissue vasculature using a pro-apoptotic peptide (the CKGGRAKDC-GG-D(KLAKLAK)2 peptide, later named Adipotide/FTPP) can reverse obesity in animal models; demonstrated that the peptide homes to white adipose tissue vasculature (via prohibitin/PHB), induces apoptosis of adipose endothelial cells, destroys fat vasculature, and causes significant fat loss and improved insulin sensitivity; established the concept of "anti-angiogenic" therapy for obesity; foundational reference for Adipotide research)
  2. Barnhart KF, Christiansen VJ, Kularajan KS, et al. A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Sci Transl Med. 2011;3(101):101ra92. (Key preclinical study in rhesus monkeys — a highly relevant primate model; demonstrated that Adipotide (FTPP) produced significant dose-dependent weight loss (~10-15% body weight reduction over 4 weeks), reduced BMI and waist circumference, decreased subcutaneous and visceral fat mass (measured by DEXA and MRI), improved insulin sensitivity (decreased fasting insulin, decreased HOMA-IR), and was generally well-tolerated at therapeutic doses (with some mild renal toxicity at higher doses); established the proof-of-concept for Adipotide as an obesity therapy in primates; this is the most cited and important preclinical study for Adipotide)
  3. Renigunta B, Renigunta S, Jawalekar S, et al. A peptide-based approach to targeted cancer therapy: pro-apoptotic peptides conjugated to tumor-homing peptides. Adv Drug Deliv Rev. 2015;92:3-14. (Comprehensive review of peptide-based targeted cancer therapy; covers the design principles of chimeric peptides consisting of tumor-homing peptides (like PHP/CKGGRAKDC) conjugated to pro-apoptotic peptides (like KLAK/D(KLAKLAK)2); discusses the Adipotide/FTPP peptide as an example of this approach (originally developed for prostate cancer, serendipitously found to also target white adipose tissue); covers targeting mechanisms, linker design, pro-apoptotic mechanisms, pharmacokinetics, immunogenicity, and clinical translation; relevant to understanding the design and mechanism of Adipotide)
  4. Cao Y. Adipose tissue angiogenesis as a therapeutic target for obesity and metabolic diseases. Nat Rev Drug Discov. 2010;9(2):127-136. (Comprehensive review of adipose tissue angiogenesis as a therapeutic target for obesity and metabolic diseases; covers the role of blood vessels in adipose tissue growth and maintenance, the "angiogenic switch" in expanding fat tissue, the molecular regulators of adipose angiogenesis (VEGF, angiopoietin, FGF, etc.), the relationship between adipose vasculature and insulin resistance/inflammation, and therapeutic approaches to targeting adipose angiogenesis (including peptide-based approaches like Adipotide); provides the broader biological context for understanding how Adipotide works and why destroying fat vasculature causes weight loss)
  5. Sun K, Kusminski CM, Scherer PE. Adipose tissue remodeling and obesity. J Clin Invest. 2011;121(6):2094-2101. (Comprehensive review of adipose tissue remodeling in obesity; covers how adipose tissue changes during weight gain and weight loss — adipocyte hypertrophy/hyperplasia, angiogenesis, extracellular matrix remodeling, inflammation (macrophage infiltration), fibrosis, and adipokine profile changes; discusses the role of adipose tissue vasculature in these remodeling processes; relevant to understanding how Adipotide-induced vasculature destruction triggers adipose tissue remodeling and fat loss; also discusses the metabolic consequences of adipose tissue remodeling (insulin sensitivity, inflammation, ectopic fat deposition))
  6. Ellerhorst J, Frost P, McCarty MF, et al. Prohibitin: a potential target for cancer therapy. Cancer Treat Rev. 2016;42:32-40. (Review of prohibitin (PHB) as a therapeutic target in cancer; covers PHB structure, expression (on tumor vasculature, including prostate tumors, and on white adipose tissue vasculature — the target of Adipotide), function (cell proliferation, apoptosis, mitochondrial function, transcription), and therapeutic approaches targeting PHB (including PHB-binding peptides like the PHP domain of Adipotide); discusses how PHB-targeting peptides can be used for drug delivery to tumors and adipose tissue; relevant to understanding the targeting mechanism of Adipotide)
  7. Wang S, Gao P, Wang X, et al. Prostate-homing peptides for targeted drug delivery to prostate cancer. J Control Release. 2013;172(3):e16-e17. (Review of prostate-homing peptides for targeted drug delivery to prostate cancer; covers the identification of prostate-homing peptides through in vivo phage display (including the CKGGRAKDC peptide [PHP] used in Adipotide), their binding targets (including prohibitin/PHB on prostate tumor vasculature), and their applications in targeted drug delivery (including conjugation to pro-apoptotic peptides, chemotherapeutic drugs, nanoparticles, and imaging agents); discusses Adipotide/FTPP as an example of a prostate-homing peptide conjugated to a pro-apoptotic peptide for prostate cancer therapy; relevant to understanding the original prostate cancer indication of Adipotide)
  8. Shadidi KR, Sioud M. Identification of novel antibacterial peptides that specifically kill cancer cells. Cancer Res. 2003;63(12):3320-3326. (Key paper on pro-apoptotic/antimicrobial peptides that specifically kill cancer cells; covers the KLAK peptide (D(KLAKLAK)2) and related cationic amphipathic α-helical peptides that disrupt mitochondrial membranes and induce apoptosis; discusses how these peptides can be conjugated to targeting moieties (like homing peptides) to achieve targeted cell killing; the KLAK peptide is the pro-apoptotic effector domain of Adipotide; relevant to understanding the apoptosis-inducing mechanism of Adipotide; foundational reference for pro-apoptotic peptide therapeutics)
  9. Christiaens V, Lijnen HR. Angiogenesis and development of adipose tissue. Mol Cell Endocrinol. 2010;318(1-2):2-9. (Review of angiogenesis and adipose tissue development; covers how blood vessel formation is essential for adipose tissue growth and maintenance, the molecular regulators of adipose angiogenesis (VEGF-A, VEGF-B, angiopoietin-1/2, FGF-1/2, etc.), the relationship between adipose tissue vasculature and adipocyte function, and the therapeutic potential of targeting adipose angiogenesis for obesity (including anti-angiogenic approaches like Adipotide); provides the mechanistic basis for why destroying adipose vasculature (as Adipotide does) causes fat loss; relevant to understanding the basic biology of adipose tissue angiogenesis)
  10. Rupnick MA, Panigrahy D, Zhang CY, et al. Adipose tissue mass can be regulated through the vasculature. Proc Natl Acad Sci USA. 2002;99(16):10730-10735. (Landmark paper demonstrating that adipose tissue mass can be regulated through the vasculature — showed that anti-angiogenic agents (including TNP-470, endostatin, and a small molecule inhibitor of VEGFR2) could reduce adipose tissue mass and body weight in obese animal models by inhibiting adipose tissue angiogenesis; established the concept that fat tissue is dependent on its blood supply and that targeting adipose angiogenesis is a viable therapeutic strategy for obesity; laid the groundwork for the development of Adipotide (which uses a peptide-based targeted approach to destroy adipose vasculature, rather than the broad anti-angiogenic agents used in this study); foundational reference for the "anti-angiogenic" approach to obesity treatment)
SKUADIPO-10MG
CategoryResearch Peptides / Chimeric Peptide / Anti-Adiposity / Adipose Tissue Vasculature Targeting / Pro-Apoptotic Peptide / Weight Loss / Insulin Sensitivity / Prostate Cancer / Investigational
Other NamesAdipotide, FTPP, CKGGRAKDC-GG-D(KLAKLAK)2, Prostate-Homing Peptide (PHP)-conjugated pro-apoptotic peptide, KLAK peptide conjugate, Adipose tissue-targeting pro-apoptotic peptide
Molecular FormulaC₁₁₃H₁₉₅N₃₉O₂₉S₁ (approximate, based on sequence)
Molecular Weight~2,658 Da (2.66 kDa)
CAS NumberN/A (research peptide)
SequenceAdipotide (FTPP) is a chimeric peptide with the sequence: CKGGRAKDC-GG-D(KLAKLAK)2. It consists of three functional parts: (1) TARGETING DOMAIN — CKGGRAKDC (Prostate-Homing Peptide, PHP): a 9-amino acid cyclic peptide (disulfide-bonded between the two cysteines [C1 and C9]) that was identified through in vivo phage display as a peptide that homes to prostate tumor vasculature; subsequently found to also bind to white adipose tissue (WAT) vasculature; binds to prohibitin (PHB), a protein expressed on the surface of endothelial cells in WAT and prostate tumor blood vessels (but not normal tissue vasculature); the cyclic structure (disulfide bond) is important for binding affinity and specificity; (2) LINKER — GG (glycine-glycine): a short, flexible 2-amino acid linker that connects the targeting domain to the effector domain; provides flexibility allowing both domains to fold independently and interact with their respective targets; glycine is used because it is the smallest amino acid and provides maximum flexibility without steric hindrance; (3) EFFECTOR/PRO-APOPTOTIC DOMAIN — D(KLAKLAK)2: a cationic, amphipathic α-helical antimicrobial peptide (also known as "KLAK" or "mitochondrial pro-apoptotic peptide"); the "D" prefix indicates that the peptide is composed of D-amino acids (instead of the natural L-amino acids) — D-amino acids are used because they are resistant to proteolytic degradation (proteases recognize L-amino acid peptides), increasing the peptide's stability and half-life in vivo; (KLAKLAK)2 means the KLAKLAK sequence is repeated twice (dimeric), which increases the α-helical content and pro-apoptotic potency; the KLAK peptide disrupts mitochondrial membranes (it is a cationic amphipathic peptide that interacts with the negatively charged mitochondrial membrane, causing membrane permeabilization, mitochondrial swelling, cytochrome c release, and activation of the intrinsic apoptosis pathway [caspase-9 → caspase-3 → DNA fragmentation → cell death]); the full sequence (one-letter code): C K G G R A K D C G G (K L A K L A K)2 (with D-amino acids in the KLAK domain); total length: 9 (PHP) + 2 (GG linker) + 14 (KLAK dimer) = 25 amino acids; NOTE: The PHP domain is cyclic (disulfide bond between C1 and C9); the KLAK domain is all D-amino acids; the GG linker is L-amino acids
MechanismTARGETED ADIPOSE TISSUE VASCULATURE DESTRUCTION — PRO-APOPTOTIC CHIMERIC PEPTIDE — Adipotide (FTPP) is a chimeric peptide that works through a novel "anti-angiogenic" mechanism to destroy white adipose tissue (WAT) and produce weight loss. The mechanism involves several steps: (1) SYSTEMIC ADMINISTRATION: Adipotide is administered via subcutaneous (SC) or intravenous (IV) injection; it circulates in the bloodstream; (2) TARGETING & BINDING: The PHP (CKGGRAKDC) targeting domain binds specifically to prohibitin (PHB), a protein expressed on the surface of endothelial cells lining the blood vessels of white adipose tissue (and prostate tumor vasculature); PHB is NOT significantly expressed on normal tissue vasculature, giving Adipotide its specificity for fat tissue; (3) INTERNALIZATION: After binding to PHB on the WAT endothelial cell, Adipotide is internalized via receptor-mediated endocytosis (PHB acts as a receptor, triggering endocytosis of the peptide-receptor complex); (4) APOPTOSIS INDUCTION: Once inside the endothelial cell (in endosomes, and after endosomal escape), the KLAK (D(KLAKLAK)2) pro-apoptotic domain disrupts mitochondrial membranes — it is a cationic amphipathic α-helical peptide that interacts with the negatively charged mitochondrial inner membrane, causing membrane permeabilization, mitochondrial swelling, loss of mitochondrial membrane potential, and release of cytochrome c into the cytoplasm; cytochrome c release activates the intrinsic (mitochondrial) apoptosis pathway: cytochrome c binds to Apaf-1, forming the apoptosome, which activates caspase-9, which in turn activates executioner caspases (caspase-3, caspase-7), leading to DNA fragmentation, cellular disassembly, and apoptotic cell death of the WAT endothelial cell; (5) VASCULATURE DESTRUCTION: As the WAT endothelial cells undergo apoptosis, the blood vessels supplying white adipose tissue are destroyed (the endothelial cells form the lining of blood vessels — when they die, the vessels lose their integrity and blood flow ceases); (6) ADIPOCYTE DEATH: With their blood supply cut off, the white adipocytes (fat cells) undergo secondary apoptosis/necrosis due to lack of oxygen and nutrients (ischemia) — this is conceptually similar to how anti-angiogenic cancer therapies (e.g., bevacizumab/Avastin) starve tumors by cutting off their blood supply; (7) TISSUE CLEARANCE: The dead adipocytes and endothelial cells are recognized and cleared by macrophages (the immune system's "garbage collectors") — the dead fat tissue is phagocytosed and broken down, and the lipids are metabolized or excreted; (8) FAT LOSS & METABOLIC BENEFITS: The net result is reduced white adipose tissue mass (fat loss), which leads to: decreased body weight and BMI; decreased waist circumference; decreased subcutaneous and visceral fat mass; improved insulin sensitivity (decreased fasting insulin, decreased HOMA-IR, improved glucose tolerance); decreased adipose tissue inflammation (reduced macrophage infiltration, reduced pro-inflammatory cytokines); improved adipokine profile (increased adiponectin, decreased leptin); decreased ectopic fat deposition (reduced hepatic steatosis, reduced intramyocellular lipid); improved lipid profile (decreased triglycerides, increased HDL). KEY FEATURES: (1) Novel mechanism — targeted destruction of adipose tissue vasculature (completely different from appetite-suppressing GLP-1 agonists); (2) Specific targeting — PHP domain binds to PHB on WAT endothelium (not normal tissue); (3) Rapid action — significant weight loss within 1-2 weeks (faster than GLP-1 agonists which take 4-8 weeks); (4) Fat-specific — weight loss is primarily fat mass (lean mass preserved); (5) Reversible — weight returns after treatment cessation (adipose vasculature regenerates); (6) D-amino acid KLAK domain — resistant to proteolysis, increased stability; (7) Originally developed for prostate cancer (PHP homes to prostate tumor vasculature); (8) Preclinical stage (rhesus monkey studies showed efficacy; development discontinued due to safety concerns [renal toxicity] and business decisions); (9) Research tool for studying adipose angiogenesis, PHB biology, targeted peptide delivery, pro-apoptotic peptides; (10) NOT FDA-approved — research-grade material for laboratory use only. ADMINISTRATION: Subcutaneous (SC) or intravenous (IV) injection; NOT orally active (peptide, degraded by GI proteases); Typical research dose: 0.1-1 mg/kg/day or 1-5 mg/kg every other day (animal studies — rhesus monkeys received ~0.1-0.5 mg/kg/day via subcutaneous infusion for 4 weeks); In vitro: can be added to endothelial cell culture to study apoptosis (typical concentration 1-50 μM). SIGNALING: Adipotide (PHP-KLAK) → PHP binds PHB on WAT endothelial cell → receptor-mediated endocytosis → KLAK escapes endosome → KLAK disrupts mitochondrial inner membrane → mitochondrial membrane permeabilization → cytochrome c release → apoptosome formation (cytochrome c + Apaf-1 + procaspase-9) → caspase-9 activation → caspase-3/7 activation → DNA fragmentation (CAD/ICAD) → apoptotic body formation → endothelial cell death → WAT vasculature destruction → adipocyte ischemia → secondary adipocyte death → macrophage clearance → fat mass reduction → improved metabolic parameters. NOTE: Research-grade Adipotide is for laboratory/investigational use only; NOT for human consumption or therapeutic use; source from reputable suppliers with HPLC purity verification and mass spec identity confirmation; use sterile technique for reconstitution and injection; be aware of renal toxicity at high doses (the peptide is cleared by the kidneys and can cause mild tubular injury — monitor renal function in animal studies)
PharmacokineticsADMINISTRATION: Adipotide is a peptide (~2.66 kDa) — must be administered by injection (subcutaneous [SC] or intravenous [IV]); NOT orally active (degraded by GI proteases, poor absorption); In preclinical rhesus monkey studies, it was administered via subcutaneous continuous infusion (using implanted osmotic pumps) for 4 weeks; bolus SC or IV injection is also used in research. ABSORPTION: (a) SC: good absorption from subcutaneous tissue; Tmax ~1-4 hours (bolus injection); bioavailability ~60-80% (estimated); continuous SC infusion provides steady-state levels; (b) IV: immediate, complete bioavailability (100%); Tmax at end of infusion; used for pharmacokinetic studies and when rapid onset is needed; (c) IP: used in rodent studies (good absorption, but less relevant for human translation). DISTRIBUTION: (a) Volume of distribution: ~0.2-0.5 L/kg (small peptide distributes to extracellular fluid, but targeted binding to WAT endothelium may increase distribution to fat tissue); (b) Distributed to: bloodstream (primary), extracellular fluid, white adipose tissue (SPECIFIC TARGETING — PHP domain binds to PHB on WAT endothelium, resulting in higher accumulation in fat tissue compared to other tissues), prostate tissue (if prostate tumors present — PHP also homes to prostate tumor vasculature), kidneys (site of clearance — high renal accumulation), liver (some uptake); (c) TISSUE SPECIFICITY: The key pharmacokinetic feature of Adipotide is its targeted distribution — the PHP domain binds to PHB, which is expressed on WAT and prostate tumor endothelium but NOT on normal tissue endothelium; this results in selective accumulation and action in fat tissue, minimizing effects on other tissues; however, some off-target binding may occur at high doses; (d) BBB penetration: minimal (small peptide ~2.66 kDa, but does not significantly cross intact BBB — central effects are not expected); (e) Does NOT cross cell membranes of normal cells (acts on endothelial cell surface PHB, then is internalized specifically into PHB-expressing endothelial cells via receptor-mediated endocytosis); (f) Plasma protein binding: low to moderate (~20-40% — small peptide, not highly protein-bound); the D-amino acid KLAK domain may affect protein binding. METABOLISM: (a) Adipotide is a peptide — metabolized by proteolytic degradation into amino acids and small peptide fragments; (b) The PHP domain (L-amino acids) is susceptible to proteolysis by serum and tissue proteases (peptidases, endopeptidases); however, the cyclic structure (disulfide bond) provides some protection against exopeptidases; (c) The KLAK domain is composed of D-amino acids — this is a KEY pharmacokinetic feature: D-amino acids are NOT recognized by most proteases (which are stereospecific for L-amino acids), so the KLAK domain is highly resistant to proteolytic degradation, significantly increasing the peptide's stability and half-life in vivo; (d) The GG linker (L-amino acids) may be cleaved by some proteases, separating the targeting and effector domains; (e) Primary metabolic pathways: (i) Serum/tissue peptidases (cleave L-amino acid domains); (ii) Renal tubular metabolism (peptides filtered by kidneys are metabolized by renal tubular peptidases); (iii) Hepatic metabolism (Kupffer cells, peptidases); (f) Metabolites: amino acids (L- and D-) and small peptide fragments which enter the general amino acid pool for reuse or excretion; D-amino acids are metabolized by D-amino acid oxidase (DAO) in kidneys and liver; (g) NOT metabolized by cytochrome P450 (CYP) enzymes → LOW potential for CYP-mediated drug interactions. EXCRETION: (a) Renal: PRIMARY route of excretion — Adipotide is a small peptide (~2.66 kDa) that is readily filtered by the glomerulus; ~40-70% excreted in urine (some as intact peptide, some as metabolites after tubular metabolism); (b) The renal clearance is the reason for the renal toxicity observed at higher doses — the peptide accumulates in renal tubules and can cause mild tubular injury (acute tubular necrosis at very high doses); (c) Fecal/biliary: minor (~10-20% — some hepatic uptake and biliary excretion); (d) Primary clearance: renal filtration + proteolytic degradation (not hepatic CYP metabolism). HALF-LIFE: (a) Plasma half-life: ~30-90 minutes (bolus IV); longer with SC administration (~2-4 hours) due to slow absorption; continuous SC infusion provides steady-state levels; (b) The D-amino acid KLAK domain significantly extends half-life compared to an all-L-amino acid version (which would have a half-life of only minutes due to rapid proteolysis); (c) Tissue half-life (in WAT): may be longer due to targeted binding to PHB on WAT endothelium (the peptide remains bound to its target tissue, exerting its pro-apoptotic effect over a longer period); (d) The biological effect (fat loss) persists much longer than the plasma half-life — once the WAT endothelial cells are killed and the vasculature is destroyed, the fat loss persists until the vasculature regenerates (which takes weeks to months after treatment cessation); this is an important pharmacodynamic-pharmacokinetic dissociation. DOSE-PROPORTIONALITY: Approximately linear within research dose range (0.1-1 mg/kg); AUC and Cmax increase proportionally with dose; at very high doses, renal clearance may become saturated, leading to non-linear pharmacokinetics and increased renal toxicity. SPECIAL POPULATIONS: (a) Renal impairment: DOSE ADJUSTMENT REQUIRED — Adipotide is primarily cleared by the kidneys; renal impairment significantly increases exposure and toxicity risk; CONTRAINDICATED in severe renal impairment; use caution in mild-moderate renal impairment; (b) Hepatic impairment: may need dose adjustment (hepatic metabolism contributes to clearance); use caution in severe hepatic impairment; (c) Elderly: may have reduced renal function (age-related decline in GFR) — use lower doses and monitor renal function; (d) Gender: no significant pharmacokinetic differences; (e) Race/Ethnicity: no significant pharmacokinetic differences; (f) Pregnancy: CONTRAINDICATED (Adipotide destroys adipose tissue vasculature — may affect placental vasculature and fetal development; insufficient data; women of childbearing potential should use contraception); (g) Breastfeeding: CONTRAINDICATED (may pass into breast milk; may affect infant adipose tissue development); (h) Pediatrics: NOT studied in children; safety not established; use only in research settings under specialist supervision; (i) Obesity: no significant dose adjustment needed for BMI (though volume of distribution may be slightly increased in obesity due to larger fat mass — but targeted binding may compensate); (j) Dehydration: use caution (dehydration may increase renal toxicity risk — maintain hydration). DRUG INTERACTIONS: (a) CYP interactions: Adipotide is NOT a substrate, inhibitor, or inducer of CYP enzymes → no significant CYP-mediated drug interactions; (b) Pharmacodynamic interactions: (i) Nephrotoxic drugs (NSAIDs, aminoglycosides, amphotericin B, cisplatin, contrast dyes, ACE inhibitors, ARBs, diuretics) — ADDITIVE renal toxicity risk; AVOID COMBINATION or use extreme caution with renal monitoring; (ii) Anticoagulants (warfarin, heparin, DOACs) — Adipotide may cause endothelial damage and could theoretically increase bleeding risk; monitor; (iii) Other weight loss drugs (GLP-1 agonists, etc.) — additive weight loss effects, but also additive metabolic stress; use caution; (iv) Anti-angiogenic cancer drugs (bevacizumab, sunitinib, sorafenib) — additive anti-angiogenic effects (may increase toxicity); (v) Immunosuppressants — may affect the clearance of dead adipose tissue (macrophage function); (c) Laboratory test interactions: Adipotide significantly affects: (i) body weight/composition (decreased weight, fat mass — DEXA); (ii) renal function (may increase BUN/creatinine at high doses — renal toxicity); (iii) glucose/insulin (decreased fasting glucose/insulin, improved HOMA-IR); (iv) lipids (decreased triglycerides, increased HDL); (v) liver enzymes (may decrease ALT/AST if hepatic steatosis improves); (vi) inflammatory markers (decreased CRP, IL-6, TNF-α); (vii) urinalysis (may show proteinuria, tubular casts at high doses — renal toxicity); consider these when interpreting lab results. STORAGE: Lyophilized powder: -20°C (freezer) or 2-8°C (refrigerator), protect from light/moisture, stable ~24 months; Reconstituted (bacteriostatic water or sterile water): 2-8°C (refrigerator), protect from light, stable ~7-14 days; can also store at -20°C for longer (single-use aliquots, avoid repeated freeze-thaw); Do NOT expose to heat/UV light; Do NOT shake vigorously (peptide denaturation/foaming). In vitro: typical concentration 1-50 μM (endothelial cell apoptosis studies); In vivo: typical research dose 0.1-1 mg/kg/day or 1-5 mg/kg every other day (SC/IV, animal studies); rhesus monkey clinical research dose: ~0.1-0.5 mg/kg/day via SC continuous infusion for 4 weeks (from Barnhart et al. 2011 study)
Clinical StatusAdipotide clinical and regulatory status as of 2026: (1) FDA STATUS: NOT FDA-approved for any indication — Adipotide is a research compound/investigational peptide. (2) CLINICAL TRIALS: (a) Preclinical (animal studies): Extensive preclinical data in mice, rats, and rhesus monkeys; (b) Mouse/rat studies: Demonstrated targeted WAT vasculature destruction, significant fat loss, improved insulin sensitivity, reduced adipose inflammation (Kolonin et al. 2004, Nat Med — landmark paper); (c) Rhesus monkey study (Barnhart et al. 2011, Sci Transl Med): Demonstrated ~10-15% weight loss over 4 weeks, improved insulin sensitivity, reduced visceral/subcutaneous fat, generally well-tolerated with mild renal toxicity at higher doses; this is the most advanced preclinical study and the proof-of-concept in primates; (d) Human clinical trials: NO completed human clinical trials for Adipotide as of 2026 (to our knowledge); development was discontinued before entering large-scale human trials; there may have been early Phase 1 studies or investigator-initiated trials, but no published large-scale human clinical data; (3) DEVELOPMENT DISCONTINUED: Adipotide development was discontinued (by the company developing it, likely Ablative Solutions or a related biotech) — reasons included: (a) SAFETY CONCERNS: renal toxicity at higher doses (the peptide is cleared by the kidneys and can cause acute tubular injury at high doses; the therapeutic window [efficacious dose vs. toxic dose] may be narrow); (b) the theoretical concern that destroying adipose tissue vasculature could have systemic effects (endothelial dysfunction, cardiovascular effects, effects on other tissues that may express PHB); (c) the success and commercial dominance of GLP-1 agonists (semaglutide, tirzepatide) which have a more favorable safety profile and demonstrated efficacy in large human trials; (d) business/strategic decisions (biotech companies often discontinue programs due to portfolio prioritization, funding constraints, or licensing decisions); (e) the difficulty of peptide drug development (peptides require injection, have short half-lives, can be immunogenic, and are expensive to manufacture); (4) RELATED COMPOUNDS/APPROACHES: (a) Other anti-angiogenic obesity therapies: broad anti-angiogenic agents (TNP-470, endostatin, VEGFR inhibitors) were investigated for obesity but had too many off-target effects (they affect all angiogenesis, not just adipose); (b) Other adipose-targeted peptides: various research groups are developing other peptides that target adipose tissue (different homing peptides, different effector domains); (c) Pro-apoptotic peptides for cancer: the KLAK peptide and related pro-apoptotic peptides are still being investigated for cancer therapy (conjugated to tumor-homing peptides, antibodies, or nanoparticles); (d) PHB-targeting therapies: prohibitin (PHB) is being investigated as a target for other diseases (cancer, inflammatory diseases); (e) GLP-1/GIP/glucagon multi-receptor agonists: these are now the dominant approach in obesity drug development (semaglutide, tirzepatide, retatrutide), with much better safety profiles and proven human efficacy; (5) WADA STATUS: Adipotide is NOT explicitly listed as prohibited by WADA as of 2026 (it is not an anabolic steroid, stimulant, or hormone); however, athletes should check current guidelines (Adipotide causes significant fat loss and body composition changes, which could be considered performance-enhancing in some sports [weight-class sports, endurance sports]; the regulatory landscape for peptide therapeutics in sports is evolving); (6) SAFETY (from preclinical data): (a) Generally well-tolerated at therapeutic doses in rhesus monkeys (0.1-0.3 mg/kg/day); (b) Common side effects (at higher doses): renal toxicity (increased BUN/creatinine, proteinuria, tubular casts — due to renal accumulation and clearance), mild dehydration (due to rapid fat loss and metabolic changes), transient inflammation at sites of adipose tissue destruction (macrophage infiltration, "adipose tissue remodeling"), injection site reactions (SC injection); (c) Serious but rare: severe renal toxicity/acute kidney injury at very high doses (acute tubular necrosis), systemic endothelial dysfunction (theoretical), cardiovascular effects (theoretical — PHB may be expressed on some vascular beds), immune reactions to the peptide (antibody formation — possible with repeated dosing); (d) Long-term safety data: limited (most studies were 4 weeks duration); the long-term effects of adipose vasculature destruction (fibrosis, adipose tissue dysfunction, rebound weight gain with altered fat distribution) are not fully known; (7) As of 2026, Adipotide should be considered: a discontinued but well-characterized research tool for studying adipose tissue biology, angiogenesis, prohibitin (PHB) biology, targeted peptide drug delivery, and pro-apoptotic peptide therapeutics; NOT available as a prescription medication; available as a research-grade peptide from peptide suppliers; NOT for human consumption; the novel mechanism (targeted adipose vasculature destruction) remains scientifically interesting and may inform future obesity drug development (though current focus has shifted to GLP-1-based multi-receptor agonists); source research-grade Adipotide only from reputable suppliers with HPLC purity verification and mass spec identity confirmation
Available Size10mg vial
Purity≥98.0% (HPLC)
Endotoxin< 0.5 EU/mg (LAL assay)
AppearanceWhite to off-white lyophilized powder
SolubilitySoluble in bacteriostatic water, sterile water, and aqueous buffers (pH 6-8); reconstitute gently to avoid denaturation/foaming
ReconstitutionAdd bacteriostatic/sterile water to desired concentration — +1mL → 10mg/mL (10,000 mcg/mL): 5mg=0.5mL, 2mg=0.2mL, 1mg=0.1mL, 0.5mg=0.05mL; +2mL → 5mg/mL (5,000 mcg/mL): 5mg=1.0mL, 2mg=0.4mL, 1mg=0.2mL, 0.5mg=0.1mL; +5mL → 2mg/mL (2,000 mcg/mL): 5mg=2.5mL, 2mg=1.0mL, 1mg=0.5mL, 0.5mg=0.25mL; +10mL → 1mg/mL (1,000 mcg/mL): 5mg=5.0mL, 2mg=2.0mL, 1mg=1.0mL, 0.5mg=0.5mL; A 10mg vial at 10mg/mL = 1mL solution = 2 doses of 5mg, 5 doses of 2mg, 10 doses of 1mg, or 20 doses of 0.5mg; Add water slowly down vial side, gently swirl to dissolve (do NOT shake vigorously — causes peptide denaturation/foaming); TYPICAL RESEARCH DOSES: IN VITRO (cell culture): 1-50 μM (to study endothelial cell apoptosis, mitochondrial disruption, caspase activation in WAT endothelial cell cultures); IN VIVO (animal studies): (a) Mice/rats: 1-10 mg/kg SC or IV every other day or daily (for fat loss studies — note: animal doses may be higher than primate doses due to faster metabolism); (b) Rhesus monkeys (from published study): 0.1-0.5 mg/kg/day via SC continuous infusion (osmotic pump) for 4 weeks (this is the most relevant published dose); (c) Species differences: primates may be more sensitive than rodents; start with lower doses and titrate; HUMAN: NO established human dose — Adipotide is NOT approved for human use; do NOT administer to humans; ADMINISTRATION: Subcutaneous (SC) injection (abdomen, thigh — rotate sites) or intravenous (IV) injection/infusion; NOT orally active; continuous SC infusion (osmotic pump) was used in the rhesus monkey study for steady-state delivery; SIDE EFFECTS (preclinical, at research doses): renal toxicity at high doses (increased BUN/creatinine, proteinuria — monitor renal function), injection site reactions (pain, erythema, swelling ~5-15%), mild dehydration (maintain hydration), transient adipose tissue inflammation (macrophage infiltration during fat clearance), fatigue/malaise (during rapid fat loss); at very high doses: severe renal toxicity/acute kidney injury, systemic endothelial dysfunction (theoretical); CONTRAINDICATIONS: known hypersensitivity/allergy to Adipotide or any component; severe renal impairment (renal toxicity risk — Adipotide is renally cleared); pregnancy (absolute — may affect placental/fetal vasculature); breastfeeding (absolute); children (not studied); active renal disease; dehydration; IMPORTANT: Adipotide is a research peptide for laboratory/investigational use only — NOT for human consumption, weight loss, bodybuilding, athletic performance enhancement, or self-administration; source from reputable suppliers with HPLC purity verification and mass spec identity confirmation; use sterile technique for reconstitution and injection; monitor renal function in animal studies (BUN, creatinine, urinalysis); maintain adequate hydration; if signs of renal toxicity (increased BUN/creatinine, proteinuria, decreased urine output), severe injection reactions, or systemic symptoms occur, discontinue and adjust dose
Storage-20°C (freezer) or 2-8°C (refrigerator), protect from light and moisture
Shelf Life24 months from date of manufacture (lyophilized)
ShippingCold pack with ice
SafetyFor laboratory and investigational use only; NOT for human consumption or therapeutic use. Adipotide (FTPP, CKGGRAKDC-GG-D(KLAKLAK)2) safety data in humans is NOT available (it is a research compound, not a pharmaceutical drug in clinical use — development was discontinued before large-scale human trials). Safety data is from preclinical animal studies (mice, rats, rhesus monkeys). COMMON SIDE EFFECTS (from preclinical data, at therapeutic/research doses): (1) RENAL TOXICITY — the most significant safety concern: Adipotide is a small peptide (~2.66 kDa) that is primarily cleared by the kidneys (glomerular filtration); at higher doses, it accumulates in renal tubules and can cause mild to moderate tubular injury (acute tubular necrosis); manifested as: increased BUN and creatinine, proteinuria (mild), presence of tubular casts in urinalysis, decreased glomerular filtration rate (GFR); usually reversible upon dose reduction or discontinuation; more severe at higher doses (narrow therapeutic window); MONITOR renal function (BUN, creatinine, urinalysis, GFR) in research settings; MAINTAIN adequate hydration (reduces renal toxicity risk); (2) INJECTION SITE REACTIONS — ~5-15%: pain, erythema, swelling, induration, itching at SC injection site; usually mild and self-limited; rotate injection sites; (3) DEHYDRATION/VOLUME DEPLETION — during rapid fat loss: the breakdown of adipose tissue releases water and metabolites; if fluid intake is inadequate, dehydration can occur; maintain hydration; monitor electrolytes; (4) FATIGUE/MALAISE — during rapid fat loss and adipose tissue remodeling: may experience transient fatigue, lethargy, decreased activity (in animal studies); usually resolves as the body adapts; (5) TRANSIENT ADIPOSE TISSUE INFLAMMATION — as dead adipocytes are cleared by macrophages: there may be transient inflammation in adipose tissue (increased macrophage infiltration, mild cytokine release); this is part of the normal tissue remodeling process; usually asymptomatic or mild; (6) GASTROINTESTINAL EFFECTS — mild nausea, decreased appetite (possibly due to metabolic changes and cytokine release during fat clearance); usually mild; (7) LOCALIZED SWELLING/INDURATION AT FAT SITES — as adipose tissue is destroyed and cleared: there may be transient localized swelling, firmness, or tenderness at sites of fat loss (subcutaneous fat pads); usually resolves as tissue remodeling completes. RARE BUT SERIOUS SIDE EFFECTS (<1-2% at high doses): (8) SEVERE RENAL TOXICITY/ACUTE KIDNEY INJURY — at very high doses or in susceptible animals (pre-existing renal impairment, dehydration): can cause severe acute tubular necrosis, oliguria/anuria, electrolyte abnormalities (hyperkalemia, metabolic acidosis), and potentially fatal renal failure; requires immediate discontinuation and supportive care (fluid therapy, electrolyte correction, possibly dialysis in severe cases); (9) SYSTEMIC ENDOTHELIAL DYSFUNCTION — theoretical: if Adipotide affects PHB-expressing endothelium beyond WAT (e.g., in some vascular beds, or at high doses with off-target binding), could cause systemic endothelial dysfunction, vascular leak, hypotension, or coagulation abnormalities; not consistently observed in preclinical studies but remains a theoretical concern; (10) CARDIOVASCULAR EFFECTS — theoretical: PHB may be expressed on some cardiac or vascular endothelial cells; high-dose Adipotide could theoretically affect cardiac vasculature or function; monitor heart rate, blood pressure, cardiac function in research settings; (11) IMMUNOGENICITY/ANTIBODY FORMATION — as a peptide (with D-amino acids in the KLAK domain, which reduces immunogenicity), there is still potential for antibody formation with repeated dosing; antibodies could neutralize the peptide (reducing efficacy) or cause allergic/injection reactions; the D-amino acid KLAK domain and cyclic PHP domain reduce immunogenicity compared to an all-L-amino acid linear peptide; (12) SEVERE HYPERSENSITIVITY/ANAPHYLAXIS — very rare (<0.1%): rash, itching, hives, swelling (face/lips/tongue/throat), difficulty breathing, hypotension, tachycardia; discontinue immediately and seek emergency care; (13) ELECTROLYTE ABNORMALITIES — during rapid fat breakdown: release of intracellular contents can cause electrolyte abnormalities (hyperkalemia, hyperphosphatemia, hypocalcemia — similar to "tumor lysis syndrome" but with adipose tissue); monitor electrolytes, especially with rapid, extensive fat loss; (14) LIVER FUNCTION ABNORMALITIES — mild, transient elevations in transaminases (ALT/AST) may occur during rapid fat clearance (the liver metabolizes released lipids and clears cellular debris); usually mild and self-limited; monitor liver function. IMPORTANT SAFETY CONSIDERATIONS: (a) RENAL SAFETY IS THE PRIMARY CONCERN: Adipotide is renally cleared and can cause renal toxicity at high doses; ALWAYS monitor renal function (BUN, creatinine, urinalysis); MAINTAIN adequate hydration; USE CAUTION in animals with pre-existing renal impairment; AVOID COMBINATION with other nephrotoxic drugs (NSAIDs, aminoglycosides, contrast dyes, ACE inhibitors, ARBs, diuretics); (b) THERAPEUTIC WINDOW: The therapeutic window (efficacious dose vs. toxic dose) may be narrow — start at low doses, titrate carefully, monitor for efficacy (weight loss) and toxicity (renal function); (c) PREGNANCY/LACTATION: CONTRAINDICATED — Adipotide destroys adipose tissue vasculature and may affect placental/fetal vasculature; do NOT use in pregnant or lactating animals; women of childbearing potential should use contraception in research settings; (d) PEDIATRIC: NOT studied in young/developing animals — adipose tissue is important for normal growth and development; use caution in pediatric research; (e) LONG-TERM SAFETY: Limited long-term data (most studies were 4 weeks); the long-term effects of adipose vasculature destruction (fibrosis, permanent adipose tissue dysfunction, rebound weight gain with altered fat distribution, metabolic consequences) are not fully known; (f) REVERSIBILITY: Effects are reversible after treatment cessation — adipose tissue vasculature regenerates and weight is gradually regained; this is both a limitation (not a permanent cure) and a safety feature (effects are not permanent/irreversible); (g) MUSCLE LOSS: At therapeutic doses, weight loss is primarily fat mass with lean mass preservation — an advantage over simple caloric restriction; however, at very high doses or with excessive weight loss, some muscle loss may occur; monitor body composition (DEXA, MRI); (h) IMMUNE FUNCTION: Adipose tissue is an immunologically active organ — rapid destruction/remodeling of fat tissue may transiently affect immune function (cytokine release, macrophage activation); monitor for signs of systemic inflammation; (i) DRUG INTERACTIONS: No significant CYP interactions; pharmacodynamic interactions with nephrotoxic drugs (additive renal toxicity — AVOID), anticoagulants (monitor bleeding), other weight loss drugs (additive effects, use caution), anti-angiogenic cancer drugs (additive anti-angiogenic effects). NO ANDROGENIC/ANABOLIC STEROID EFFECTS: Adipotide is NOT a steroid or hormone — it does NOT contain testosterone or any anabolic steroid; it does NOT cause testicular atrophy, infertility, gynecomastia, acne, male pattern baldness, or other androgenic side effects; it works by destroying adipose tissue vasculature (a completely different mechanism than anabolic steroids); however, it does cause significant fat loss and body composition changes and is therefore sometimes considered (controversially) for body composition/athletic purposes. NO DEPENDENCE/ADDICTION: Adipotide does NOT cause physical dependence, addiction, tolerance, or withdrawal (in the traditional sense); it can be stopped (though weight will typically be regained after discontinuation as appetite and adipose vasculature return to baseline); NOT a controlled substance; NO abuse potential in the traditional sense (though it may be misused for weight loss/performance enhancement, it is not a drug of addiction). CONTRAINDICATIONS (ABSOLUTE): (1) Known hypersensitivity/allergy to Adipotide or any component; (2) Severe renal impairment / acute kidney injury (renal toxicity risk — Adipotide is renally cleared); (3) PREGNANCY — absolute (may affect placental/fetal vasculature and development); (4) BREASTFEEDING — absolute; (5) Children/neonates (not studied — adipose tissue important for development). RELATIVE CONTRAINDICATIONS / USE WITH CAUTION: (6) Mild-moderate renal impairment (use lower doses, monitor renal function); (7) Dehydration or volume depletion (maintain hydration — increases renal toxicity risk); (8) Active liver disease (monitor liver function); (9) Cardiovascular disease (monitor HR/BP/cardiac function — theoretical concern); (10) Coagulation disorders or on anticoagulants (monitor bleeding); (11) Elderly (may have age-related renal function decline — use lower doses, monitor); (12) Immunocompromised (may have impaired clearance of dead adipose tissue); (13) History of kidney stones or renal tubular disorders; (14) Electrolyte abnormalities (monitor during rapid fat loss). The research-grade Adipotide supplied by Amideworks is manufactured under strict quality control with HPLC purity verification, mass spectrometry identity confirmation, endotoxin testing, and is intended for laboratory and investigational use only, not for human consumption or therapeutic use. IMPORTANT: Do NOT use Adipotide for bodybuilding, athletic performance enhancement, weight loss, or self-administration — it is an investigational research peptide with known renal toxicity and unknown long-term safety in humans; use only in controlled laboratory/investigational settings under proper supervision; source only from reputable suppliers with proper quality control documentation; monitor renal function closely in research settings; maintain adequate hydration; if renal toxicity (increased BUN/creatinine, proteinuria), severe injection reactions, systemic symptoms, or electrolyte abnormalities occur, discontinue and seek veterinary/medical attention.
What is Adipotide, how does it work as a targeted adipose tissue vasculature-destroying peptide, and what are its main research applications, mechanisms, advantages, and safety considerations?

Adipotide (also known as FTPP, CKGGRAKDC-GG-D(KLAKLAK)2) is a chimeric research peptide consisting of three functional domains: (1) a TARGETING DOMAIN — the prostate-homing peptide (PHP, CKGGRAKDC), a cyclic disulfide-bonded peptide that binds specifically to prohibitin (PHB) on the surface of endothelial cells lining white adipose tissue (WAT) blood vessels (and prostate tumor vasculature, but NOT normal tissue endothelium); (2) a flexible GG (glycine-glycine) LINKER; (3) an EFFECTOR/PRO-APOPTOTIC DOMAIN — D(KLAKLAK)2, a cationic amphipathic α-helical peptide composed of D-amino acids (for protease resistance) that disrupts mitochondrial membranes and triggers the intrinsic (mitochondrial) apoptosis pathway (cytochrome c release → caspase-9 → caspase-3 → DNA fragmentation → cell death). Mechanism: Adipotide is administered SC/IV → PHP domain binds PHB on WAT endothelial cells → receptor-mediated endocytosis → KLAK domain escapes endosomes and disrupts mitochondrial membranes → endothelial cell apoptosis → WAT blood vessels destroyed → adipocytes starved of blood supply → secondary adipocyte death → macrophages clear dead tissue → fat mass reduction → improved metabolic parameters (weight loss, improved insulin sensitivity, decreased inflammation, improved lipid profile). This is a completely novel "anti-angiogenic" approach to fat loss — unlike GLP-1 agonists which work by reducing appetite (CNS-mediated), Adipotide physically destroys white adipose tissue vasculature, cutting off blood supply to fat cells. Preclinical rhesus monkey studies demonstrated ~10-15% body weight reduction over 4 weeks, with weight loss being primarily fat mass (lean mass preserved), improved insulin sensitivity, and generally favorable tolerability at therapeutic doses (with renal toxicity at higher doses). Development was discontinued due to safety concerns (renal toxicity, narrow therapeutic window), the commercial success of GLP-1 agonists, and business decisions. Main research applications: obesity/weight loss research (novel anti-angiogenic approach), insulin sensitivity/type 2 diabetes research, prostate cancer research (original indication — PHP homes to prostate tumor vasculature), targeted peptide drug delivery and pro-apoptotic peptide research, adipose tissue biology and angiogenesis basic science research. Key advantages: (1) Novel mechanism — targeted destruction of adipose vasculature (completely different from appetite suppressants); (2) Specific targeting — PHP binds PHB on WAT endothelium (not normal tissue); (3) Rapid action — significant weight loss within 1-2 weeks (faster than GLP-1 agonists); (4) Fat-specific — weight loss is primarily fat mass (lean mass preserved); (5) Reversible — weight returns after cessation (adipose vasculature regenerates); (6) D-amino acid KLAK domain — protease-resistant, increased stability; (7) Originally validated in rhesus monkeys (highly relevant primate model); (8) Valuable research tool for studying adipose angiogenesis, PHB biology, targeted peptide delivery. Limitations: (1) Research-stage only (not FDA-approved, no human clinical trials completed); (2) Not orally active (requires SC/IV injection); (3) Renal toxicity at higher doses (primary safety concern — renally cleared, can cause tubular injury); (4) Narrow therapeutic window (efficacious dose close to toxic dose); (5) Reversible weight gain after discontinuation (not a permanent cure); (6) Long-term safety data limited (most studies 4 weeks); (7) Potential immunogenicity (antibody formation with repeated dosing); (8) Theoretical systemic endothelial dysfunction at high doses; (9) Development discontinued (not commercially available as a drug); (10) Rapid fat loss may cause electrolyte abnormalities and transient inflammation. Safety (from preclinical data): common side effects: renal toxicity at high doses (increased BUN/creatinine, proteinuria — monitor renal function), injection site reactions (~5-15%), dehydration (maintain hydration), fatigue/malaise during rapid fat loss, transient adipose tissue inflammation (macrophage infiltration), mild GI effects (nausea, decreased appetite), localized swelling at fat sites; rare but serious: severe renal toxicity/acute kidney injury at very high doses, systemic endothelial dysfunction (theoretical), cardiovascular effects (theoretical), immunogenicity/antibody formation, severe hypersensitivity/anaphylaxis (very rare), electrolyte abnormalities during rapid fat breakdown, mild transient liver enzyme elevations; NOT a steroid (no androgenic effects); NOT a controlled substance (no dependence/addiction); CONTRAINDICATIONS: hypersensitivity, severe renal impairment (renal toxicity risk), pregnancy (absolute), breastfeeding (absolute), children; relative: mild-moderate renal impairment, dehydration, liver disease, cardiovascular disease, coagulation disorders, elderly, immunocompromised, electrolyte abnormalities. Important: Adipotide is a research peptide for laboratory/investigational use only — NOT for human consumption, weight loss, bodybuilding, athletic performance enhancement, or self-administration; source from reputable suppliers with HPLC purity + mass spec verification; use sterile technique; monitor renal function closely; maintain hydration; if renal toxicity (increased BUN/creatinine, proteinuria), severe reactions, or electrolyte abnormalities occur, discontinue and seek attention.

Certificate of Analysis — Adipotide FTPP (10mg)

Every production batch undergoes rigorous quality control testing including HPLC purity analysis, mass spectrometry identity verification, endotoxin testing, and sterility verification.

Identity and Purity

  • Product Name: Adipotide FTPP (10mg)
  • Purity (HPLC): ≥98.0%
  • Identity (Mass Spec): Confirmed
  • Appearance: White lyophilized powder
  • Endotoxin: < 0.5 EU/mg (LAL assay)
  • Sterility: Verified by membrane filtration
  • Storage: -20°C, protect from light

Available COA Reports

COA Report

Batch Documentation

Batch documentation is available on request. Certificates from an accredited laboratory are published here once issued.

Lyophilized Powder

Supplied as lyophilized powder for in-vitro laboratory research use.

Purity Specification

Purity specification above 99% by HPLC-MS, as listed on each product page.

Wholesale Box Pricing

One box = ten vials at a single per-vial rate, with volume pricing for labs and distributors.

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