Ruxotemitide
A nine-residue cationic peptide that punches holes in cancer cells and their mitochondria, then recruits the immune system
Ruxotemitide, better known as LTX-315, is a short positively charged peptide designed by Lytix Biopharma from lactoferricin, a germ-killing fragment of a cow's-milk protein. Injected directly into a tumour, it disrupts the membranes of cancer cells and their mitochondria, causing a messy, inflammatory death that releases danger signals and draws T cells in. In a phase 1 trial of 39 patients it shrank injected tumours by at least 30% in 29% of them but produced no formal responses, and about one in ten had a severe allergic reaction. Phase 2 trials in melanoma, sarcoma and basal cell carcinoma followed; it is not approved.
Used in human trials: 5 mg per injection (total 25-120 mg), Up to eight injections per treatment day, on three to five days, Intratumoral injection (Study: sarcoma pilot with T-cell therapy) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
Many animals defend themselves against bacteria with short, positively charged peptides that tear holes in microbial membranes. Cancer cells share one weakness with bacteria: their outer membranes carry more negative charge than those of healthy cells. Lytix Biopharma's chemists started from lactoferricin, a fragment of the milk protein lactoferrin, and through structure-activity work arrived at a nine-residue peptide rich in lysine and tryptophan with one unnatural bulky amino acid, β,β-diphenylalanine. LTX-315, given the international name ruxotemitide, killed drug-resistant and drug-sensitive cancer cells while sparing normal cells more, and lasted 160 minutes in human plasma before breaking down into non-toxic pieces.
Laboratory work showed how it kills. The peptide enters cells, gathers around mitochondria and permeabilises their membranes, stopping respiration within moments; cells lacking two pro-death proteins of the BCL-2 family, or lacking mitochondria altogether, resisted it. The death that follows is necrotic and noisy. Dying cells expose calreticulin, spill the energy molecule adenosine triphosphate and the alarm protein HMGB1, and set off a type 1 interferon response, the full set of markers of what immunologists call immunogenic cell death. That is the point of the drug: it is meant to turn a tumour into its own vaccine.
Mouse and rat studies supported the idea. Injected into B16 melanomas it caused complete regression in most animals, and cured mice rejected the same tumour when it was given again. In rats with fibrosarcoma, treating one tumour made untreated ones shrink, an abscopal effect that depended on T cells. It reduced regulatory T cells and suppressor cells in the tumour and rescued mice whose tumours resisted CTLA-4 blockade. Later work found it matures dendritic cells through TLR7 and MyD88 and lowers PD-L1 in pancreatic cancer models.
People have so far received it only in small trials. In the dose-ranging phase 1 study, 39 patients with accessible solid tumours had injections into accessible tumours. Transient drops in blood pressure (46%), flushing and injection-site reactions were common, and four patients (10%) had grade 3 hypersensitivity or anaphylaxis. Biopsies showed necrosis and more CD8 T cells in 12 of 14 tumours, and new T-cell clones expanded in the blood, but no patient met the criteria for a partial response. A six-patient pilot in sarcoma combined it with tumour-infiltrating lymphocyte therapy, and phase 2 trials have tested it with pembrolizumab in melanoma and, as VP-315, in basal cell carcinoma.
Ruxotemitide is not a peptide anyone could use outside a cancer centre. It is injected under imaging into a tumour by an oncology team that must be ready to treat anaphylaxis, and its trial doses below are what those teams used, not amounts for anyone else.
Mechanism of Action
Ruxotemitide is an oncolytic peptide: its positive charge and bulky aromatic side chains let it disrupt cancer cell and mitochondrial membranes, and the way those cells die turns on an immune response.
Drawn to cancer membranes
Five lysines give it a strong positive charge, and its tryptophans and diphenylalanine anchor it in membranes; it broke melanoma cell membranes within two hours (PMID 26472184).
Mitochondria permeabilised
It gathers in mitochondria, stops respiration and releases their contents, partly through pro-death proteins of the BCL-2 family (PMID 26378049).
Immunogenic cell death
Dying cells expose calreticulin and release adenosine triphosphate, HMGB1 and interferon signals that recruit and prime immune cells (PMID 26962684); dendritic cells are also switched on through TLR7 (PMID 38545099).
T cells reach other tumours
In animals, treating one tumour shrank distant ones through CD8 T cells (PMID 28920000); in patients, new T-cell clones expanded in blood after injections (PMID 33542073).
Published Research
The studies behind ruxotemitide (LTX-315), read from their PubMed abstracts: the phase 1 trial, a sarcoma pilot and a case report in people, two reviews by its developers' collaborators, and the animal and cell studies that worked out how it kills cancer cells.
Phase 1: 39 patients with solid tumours
Injections into accessible tumours caused transient low blood pressure in 46%, flushing in 28% and injection-site reactions in 38%; 10% had grade 3 hypersensitivity or anaphylaxis. Injected tumours shrank by at least 30% in 29% of patients and 12 of 14 biopsies gained CD8 T cells, but there were no partial responses by immune-related criteria.
Sarcoma: combined with T-cell therapy
Six heavily pretreated patients with metastatic soft tissue sarcoma received intratumoral LTX-315 and four went on to tumour-infiltrating lymphocyte therapy. Toxicity was manageable; the best result was stable disease for 208 days, and new T-cell clones, some against predicted neoantigens, appeared in blood.
Case report: a desmoid tumour
A 29-year-old woman with an unresectable desmoid tumour of the chest wall had repeated injections in the phase 1 trial. CD8 T cells and immune genes rose in the tumour, pain eased and the disease stayed stable long term; treatment stopped at week 16 after a serious allergic reaction.
First-in-class oncolytic peptide
A review describes LTX-315's design from host defence peptides, its attack on plasma and mitochondrial membranes with release of danger signals, and its reprogramming of the tumour environment toward effector T cells and away from suppressive cells in mice.
Oncopore as an immunotherapy
The developers summarise that injecting LTX-315 into B16 melanomas caused complete regression and lasting, body-wide protective immunity in mice.
Melanoma regression in mice
Injected into skin melanomas in mice, LTX-315 caused necrosis, immune cell infiltration and complete regression in most animals, raised IL-1β, IL-6 and IL-18, and cured mice resisted the tumour when it was injected again into skin or blood.
Rescue after CTLA-4 blockade failed
It cut regulatory T cells and myeloid suppressor cells in tumours and raised effector T cells; in mouse tumours that had resisted CTLA-4 antibodies, later LTX-315 injections cured animals or caused regressions, including of distant tumours.
Abscopal effect in rat sarcoma
Intratumoral treatment of rat fibrosarcoma gave complete regression and also shrank untreated distant lesions, with CD8 T cells in both; the effect depended on T cells.
Two phases of response in engineered mice
In Braf/Pten melanoma and Kras/p53 sarcoma models it acted first within minutes by wrecking tumour blood vessels, independent of lymphocytes, then over weeks through CD8 T cells; the authors report similar T-cell infiltration in patients.
Dendritic cells switched on via TLR7
In melanoma models it matured tumour dendritic cells both indirectly, through released danger signals and nucleic acids, and directly through TLR7, and its anti-melanoma immunity depended on MyD88.
PD-L1 lowered in pancreatic cancer
In mouse pancreatic cancer it reduced PD-L1 and increased lymphocytes in tumours; the authors traced this to the lipid transporter ATP11B, whose loss sends PD-L1 to be degraded.
Rabbit liver tumours after incomplete ablation
In VX2 liver tumours left behind after incomplete radiofrequency ablation, 4 mg LTX-315 produced complete necrosis and the smallest tumours, and 2 mg increased CD8 T cells and lowered regulatory T cells against controls.
Killing drug-resistant bacteria
Screened from 10,926 compounds, LTX-315 killed gram-positive and gram-negative bacteria including multidrug-resistant strains by binding membrane phosphatidylglycerol, and was effective against hypervirulent Klebsiella pneumoniae in infected mice.
Immunogenic cell death
In cells it produced all four hallmarks of immunogenic cell death: surface calreticulin, release of adenosine triphosphate, HMGB1 release and a type 1 interferon response; injected into tumours it caused haemorrhagic necrosis with T-cell and myeloid infiltration at least as well as mitoxantrone.
Discovery of the 9-mer lead
From a series of chemically modified 9-mer cationic peptides, LTX-315 had the best activity against drug-resistant and drug-sensitive cancer cells with less toxicity to normal cells, a 160-minute half-life in human plasma, non-toxic breakdown products and little CYP450 inhibition.
Mitochondria are the target
The peptide accumulated in mitochondria, halted respiration at once and released intermembrane proteins; cells lacking two pro-death BCL-2 family proteins, or stripped of mitochondria, were less sensitive.
Human melanoma cells die in two hours
In A375 melanoma cells it broke the plasma membrane and killed cells within 2 hours; at low doses it collected near mitochondria, depolarised them and released adenosine triphosphate, cytochrome c and HMGB1 within minutes.
Dosing Data
Ruxotemitide is injected into tumours by oncology teams in trials. The phase 1 abstract gives no amounts; the amounts below come from the full texts of two carded papers from the trial programme.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no regulator's label that says in what form Ruxotemitide is supplied. It is prepared and given by clinical staff, not bought and mixed at home: the next part says where.
Mixing a vial: a worked example
Nothing to mix at home, and no syringe units to work out: Ruxotemitide is prepared and given by clinical staff, by an oncology team, injected into the tumour.
In every human study carded here it was injected directly into tumours by cancer specialists, often under ultrasound guidance, with severe allergic reactions treated on the spot.
Source: PMID 33542073 and PMID 38125722 and PMID 31177991 (studies carded under Research below).
Storage before and after mixing
Unknown: no label on file says how Ruxotemitide is stored. It is kept and prepared by the hospital or clinic that gives it (see the part above); the home rules for a mixed vial in the mixing guide do not apply to it.
How it is taken
As it was given in human studies: Intratumoral injection (Up to eight injections per treatment day, on three to five days; Study: sarcoma pilot with T-cell therapy).
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: a half-life of 160 minutes in human plasma in a test tube; no in-body half-life in the abstracts read. After about five half-lives almost none is left.
How long the doses were given: Study: sarcoma pilot with T-cell therapy: Up to four weeks; Study: phase 1 programme, range used: Weeks; one patient stopped at week 16.
When effects appear: unknown; no source on this page gives a time to effect for Ruxotemitide. Results reported in the studies are under Published Research.
Source: half-life: PMID 26982623; Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: Transient low blood pressure in 46% and flushing in 28% of phase 1 patients (PMID 33542073); Injection-site reactions in 38% (PMID 33542073); Grade 3 hypersensitivity or anaphylaxis in 10% of phase 1 patients (PMID 33542073); A serious allergic reaction ended treatment at week 16 in the desmoid tumour case (PMID 31177991); Manageable, expected toxicity when combined with T-cell therapy in sarcoma (PMID 38125722). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Ruxotemitide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the human studies above”).
Interactions
Unknown: a PubMed search for human interaction studies of Ruxotemitide (reviewed 2026-10-30) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Ruxotemitide products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Ruxotemitide's expected mass, 1,439.8 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: In Clinical Trials (Not approved: Drugs@FDA (openFDA) holds no record and the EMA medicines list no entry (searched October 30, 2026)). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
From the human studies above.
Contraindications & Cautions
No label exists. These cautions follow from the trials.
Legal Status
Ruxotemitide is an investigational cancer drug with no marketing approval anywhere.
Frequently Asked Questions
?What is LTX-315?
LTX-315, now named ruxotemitide, is a nine-amino-acid peptide injected into tumours. It kills cancer cells by breaking their membranes and mitochondria, in a way meant to wake up the immune system.
?Where does it come from?
It was designed by Lytix Biopharma from lactoferricin, an antibacterial fragment of the milk protein lactoferrin, and includes one unnatural amino acid, β,β-diphenylalanine.
?Does it shrink tumours in people?
In the phase 1 trial, injected tumours shrank by at least 30% in 29% of patients, but no patient met the formal criteria for a partial response. Larger phase 2 results in melanoma and skin cancer have not yet appeared in PubMed.
?What are the main risks?
Drops in blood pressure, flushing and injection-site reactions were common, and about one patient in ten had a severe allergic reaction or anaphylaxis.
?Is VP-315 the same drug?
Yes. VP-315 is the name Verrica Pharmaceuticals used for LTX-315 in its basal cell carcinoma trial.
?Is it available?
No. It is investigational and given only in cancer trials, by injection into the tumour.
References
- [clinical-trial] Spicer J, et al. "Safety, Antitumor Activity, and T-cell Responses in a Dose-Ranging Phase I Trial of the Oncolytic Peptide LTX-315 in Patients with Solid Tumors." Clin Cancer Res, 2021;27(10):2755-2763. PMID: 33542073.
- [clinical-trial] Nielsen M, et al. "LTX-315 and adoptive cell therapy using tumor-infiltrating lymphocytes generate tumor specific T cells in patients with metastatic soft tissue sarcoma." Oncoimmunology, 2024;13(1):2290900. PMID: 38125722.
- [pubmed] Jebsen NL, et al. "Enhanced T-lymphocyte infiltration in a desmoid tumor of the thoracic wall in a young woman treated with intratumoral injections of the oncolytic peptide LTX-315: a case report." J Med Case Rep, 2019;13(1):177. PMID: 31177991.
- [review] Sveinbjørnsson B, et al. "LTX-315: a first-in-class oncolytic peptide that reprograms the tumor microenvironment." Future Med Chem, 2017;9(12):1339-1344. PMID: 28490192.
- [review] Camilio KA, et al. "LTX-315 (Oncopore™): A short synthetic anticancer peptide and novel immunotherapeutic agent." Oncoimmunology, 2014;3:e29181. PMID: 25083333.
- [pubmed] Camilio KA, et al. "Complete regression and systemic protective immune responses obtained in B16 melanomas after treatment with LTX-315." Cancer Immunol Immunother, 2014;63(6):601-13. PMID: 24676901.
- [pubmed] Yamazaki T, et al. "The oncolytic peptide LTX-315 overcomes resistance of cancers to immunotherapy with CTLA4 checkpoint blockade." Cell Death Differ, 2016;23(6):1004-15. PMID: 27082453.
- [pubmed] Nestvold J, et al. "Oncolytic peptide LTX-315 induces an immune-mediated abscopal effect in a rat sarcoma model." Oncoimmunology, 2017;6(8):e1338236. PMID: 28920000.
- [pubmed] Liao HW, et al. "LTX-315 sequentially promotes lymphocyte-independent and lymphocyte-dependent antitumor effects." Cell Stress, 2019;3(11):348-360. PMID: 31799501.
- [pubmed] Li XQ, et al. "LTX-315 triggers anticancer immunity by inducing MyD88-dependent maturation of dendritic cells." Front Immunol, 2024;15:1332922. PMID: 38545099.
- [pubmed] Tang T, et al. "Oncolytic peptide LTX-315 induces anti-pancreatic cancer immunity by targeting the ATP11B-PD-L1 axis." J Immunother Cancer, 2022;10(3). PMID: 35288467.
- [pubmed] Zhou G, et al. "Interventional Oncolytic Immunotherapy with LTX-315 for Residual Tumor after Incomplete Radiofrequency Ablation of Liver Cancer." Cancers (Basel), 2022;14(24). PMID: 36551579.
- [pubmed] Tang Y, et al. "LTX-315 is a novel broad-spectrum antimicrobial peptide against clinical multidrug-resistant bacteria." J Adv Res, 2025;76:715-729. PMID: 39793961.
- [pubmed] Zhou H, et al. "The oncolytic peptide LTX-315 triggers immunogenic cell death." Cell Death Dis, 2016;7(3):e2134. PMID: 26962684.
- [pubmed] Haug BE, et al. "Discovery of a 9-mer Cationic Peptide (LTX-315) as a Potential First in Class Oncolytic Peptide." J Med Chem, 2016;59(7):2918-27. PMID: 26982623.
- [pubmed] Zhou H, et al. "The oncolytic peptide LTX-315 kills cancer cells through Bax/Bak-regulated mitochondrial membrane permeabilization." Oncotarget, 2015;6(29):26599-614. PMID: 26378049.
- [pubmed] Eike LM, et al. "The oncolytic peptide LTX-315 induces cell death and DAMP release by mitochondria distortion in human melanoma cells." Oncotarget, 2015;6(33):34910-23. PMID: 26472184.
- [registry] ClinicalTrials.gov API v2, read October 30, 2026: NCT01058616 (phase 1 dose escalation, 14 enrolled, completed 2013); NCT01986426 (phase 1, monotherapy or with ipilimumab or pembrolizumab, 80 enrolled, completed 2018); NCT03725605 (ATLAS-IT-04, with tumour-infiltrating lymphocytes in soft tissue sarcoma, 6 enrolled, completed); NCT04796194 (phase 2 with pembrolizumab in advanced melanoma, 23 enrolled, completed July 2025); NCT05188729 (phase 2, VP-315 in basal cell carcinoma, Verrica Pharmaceuticals, 92 enrolled, completed April 2024); NCT06651151 (NeoLIPA, neoadjuvant LTX-315 with pembrolizumab in resectable stage III/IV melanoma, Oslo University Hospital, recruiting). https://clinicaltrials.gov/study/NCT06651151
- [other] ChEMBL CHEMBL4297628 (ruxotemitide; synonyms LTX-315, Oncopore, KKWWKKWDipK-NH2): full molecular formula C78H106N18O9, molecular weight 1439.82. Read October 30, 2026. https://www.ebi.ac.uk/chembl/compound_report_card/CHEMBL4297628/
- [other] US FDA, Drugs@FDA (openFDA drugsfda endpoint), searched October 30, 2026: no application for ruxotemitide or LTX-315.
Sources & Citations
Every study on this page was read from its PubMed record on October 30, 2026, and the open full texts of two papers were read for the per-injection amounts. Trial status comes from ClinicalTrials.gov, regulatory status from Drugs@FDA and the EMA medicines list, and the formula from ChEMBL, all read the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.