Endogenous Metabolite
Programmed death-ligand 1 (PD-L1) [6]

L-5-HTP blocks PD-L1 induction in cancer cells. L-5-HTP transcriptionally suppresses inducible PD-L1 expression directly rather than via transformation to related metabolites. The inhibitory effects of L-5-HTP on IFN-γ stimulated PD-L1 induction are mediated by reduced expression of RTK ligands and suppression of the downstream RTK receptor/MEK/ERK/c-JUN signaling cascade.
Researchers discovered that L-5-HTP suppressed IFN-γ-induced PD-L1 expression in tumor cells transcriptionally, and this effect was directly due to itself. Mechanistically, L-5-HTP inhibited IFN-γ-induced expression of RTK ligands and thus suppressed phosphorylation-mediated activation of RTK receptors and the downstream MEK/ERK/c-JUN signaling cascade, leading to decreased PD-L1 induction [6].

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Oxitriptan suppressed IFN-γ-induced PD-L1 surface expression in a variety of human cancer cell lines, including BXPC3 (pancreatic), A549 (lung), and SKOV3 (ovarian), in a dose-dependent manner. This was confirmed by flow cytometry and immunoblotting. Oxitriptan had little influence on constitutive PD-L1 expression in these cells. The compound inhibited PD-L1 expression at the transcriptional level, as shown by qPCR, without affecting its protein stability. Mechanistically, Oxitriptan inhibited IFN-γ-induced expression of RTK ligands (e.g., HGF, AREG, VEGFA, TGFA), which in turn suppressed the phosphorylation-mediated activation of upstream RTK receptors (c-MET and EGFR) and the downstream MEK/ERK/c-JUN signaling cascade, leading to decreased PD-L1 induction. Knockdown of c-JUN via siRNA abrogated Oxitriptan's effect on PD-L1 transcription, confirming the pathway's involvement. The addition of exogenous HGF or AREG partially rescued the Oxitriptan-mediated suppression of PD-L1. The compound's effect was direct, as its metabolites (5-HT, melatonin, 5-OH Kyn) did not replicate the inhibition of PD-L1. In an MTT-based cytotoxicity assay, Oxitriptan at concentrations up to 100 µM did not inhibit the proliferation of MC38 or CT26 mouse cancer cells. In primary T cells isolated from OT-1 mice and activated with OVA, treatment with 2 µM or 10 µM Oxitriptan did not influence PD-1 expression. [6]

Animal depression models can be created using L-5-hydroxytryptophan in animal modeling.

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\nTHE depletion by reserpine of storage in the body of 5-hydroxytryptamine (‘Serotonin’) and of the catechol amines is now well established. In reserpinized animals the peripheral part of the adrenergic system does not function owing to lack of the transmitter. This is presumably true also of the central part of the adrenergic system. However, it remains to be proved to what extent the central action of reserpine may be attributed to changes in brain catechol amines and/or 5-hydroxytryptamine.[1]

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\n\nA double-blind, placebo-controlled study of the efficacy and tolerability of 5-hydroxytryptophan (5-HTP) was conducted in 50 patients with primary fibromyalgia syndrome. All the clinical parameters studied were significantly improved by treatment with 5-HTP and only mild and transient side-effects were reported. Further controlled studies are required to define properly the value of 5-HTP in patients with primary fibromyalgia syndrome.[2]

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\n\nSix patients with myoclonus of varying cause were treated with L-5-hydroxytryptophan (L-5-HTP) and carbidopa. While spontaneous myoclonus decreased in three of the patients and action myoclonus in four, only two patients had marked functional improvement. Side effects included gastrointestinal and affective disturbances. L-5-HTP therapy caused a diminished frequency of paroxysmal discharges in the electroencephalograms of three patients which did not always correlate with clinical improvement. Lumbar cerebrospinal fluid 5-hydroxyindoleacetic acid (5-HIAA) concentration after probenecid was decreased in all patients prior to therapy, but this reduction did not predict treatment response. Urinary excretion patterns for 5-HTP, serotonin, and 5-HIAA during treatment were similar in responders and nonresponders. It is concluded that while some patients with myoclonus do benefit from L-5-HTP therapy, biochemical and electrophysiological tests are not useful predictors of treatment response, and the high incidence of side effects limits the usefulness of this therapy.[3]\n

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\nThe clinical effects of the protracted treatment with 5-OH Tryptophane (5-HTP) of some patients with chronic migraine are compared with other patients with acetylsalicylic acid. The pain threshold was neurophysiologically determined in migraneous on patients whose response to 5-HTP therapy was specially good. The results with 5-HTP can be accounted for by an action of the substance on the serotonin turnover with activation of the serotoninergic antinociceptive system.[4]\n

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\nSome features of cerebellar ataxia have been reported to regress partially with long-term administration of 5-hydroxytryptophan or levorotatory form of 5-hydroxytryptophan. To test this effect further, 30 patients with various inherited or acquired cerebellar ataxias underwent a randomized, double-blind trial of placebo, and the levorotatory form of 5-hydroxytryptophan taken orally for four months. The levorotatory form of 5-hydroxytryptophan significantly improved the ataxia score. It also significantly modified the time of standing upright, the spread of feet, the speed of walking, speaking, and writing. In five cases in which the levorotatory form of 5-hydroxytryptophan therapy was maintained for 12 months, the effect continued progressively.[5]\n

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\nL-5-HTP reduces PD-L1 expression and tumor growth in vivo [6]
\nWe next investigated the potential immunotherapeutic effects of L-5-HTP. First, we determined that L-5-HTP does not have any significant deleterious effects on the proliferation of OVA-activated primary T cells isolated from an OT-Ⅰ mouse (online supplemental figure S4A). We then tested for any in vivo antitumor effects of L-5-HTP in immunocompetent mouse models. Two immunogenic mouse colon cancer cell lines (MC38 and CT26) were subcutaneously implanted into immunocompetent mice, which were given daily intraperitoneal injections of 100 mg/kg L-5-HTP. Compared with the vehicle control, L-5-HTP treatment significantly delayed the growth of both MC38 and CT26 tumors and reduced tumor weight (figure 4A, B). No significance in body weight were detected between the vehicle group and the treated group (figure 4C), suggesting that L-5-HTP was well tolerated. Moreover, the L-5-HTP treated group showed significantly better survival over the vehicle control group in both MC38 and CT26 tumor models (figure 4D). We also confirmed the antitumor therapeutic effects of L-5-HTP by showing that delaying the start of treatment until tumors reached 5 mm×5 mm (online supplemental figure S4B–D) resulted in similar suppression of tumor growth.

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In immunocompetent syngeneic mouse models (MC38 in C57BL/6 mice and CT26 in BALB/c mice), daily intraperitoneal administration of Oxitriptan at 100 mg/kg significantly delayed tumor growth, reduced tumor weight, and improved survival compared to vehicle controls. Body weight was not affected, indicating good tolerability. Flow cytometry and IHC analysis of tumors from treated mice showed reduced PD-L1 expression on tumor cells, as well as on CD11c+ MHC-II+ DCs and CD11b+ F4/80+ macrophages. Pd-l2 mRNA expression in tumors was also downregulated. Oxitriptan treatment increased the number of intratumoral CD3+ T cells, CD8+ cytotoxic T cells, and the ratio of granzyme B+ CD8+ activated cytotoxic T cells. The antitumor effect of Oxitriptan was dependent on an intact immune system, as it was not observed in immunocompromised nude mice. Furthermore, the effect was dependent on PD-L1 expression, as Oxitriptan inhibited the growth of MC38 wild-type tumors but had no effect on MC38 PD-L1 knockout (Pd-l1-/-) tumors. In a chronic social defeat stress (CSDS)-conditioned tumor mouse model, Oxitriptan administration significantly impeded tumor growth and relieved depressive-like behaviors, as measured by the tail suspension test (TST) and sucrose preference test (SPT). [6]

RNA sequencing and bioinformatic analysis [6]
BXPC3 cells were treated with one of four treatments—DMSO, IFN-γ, L-5-HTP (10 µM), and IFN-γ+L-5-HTP (10 µM)—for 24 hours. Three biological replicates were performed. Total RNA was extracted to prepare cDNA libraries, which were sequenced on the Illumina HiSeq 2000 platform using the paired-end approach. The sequencing reads were mapped to hg19 using STAR 2.5, and gene expression was quantified using the featureCounts software. Differential gene expression analysis was performed using the DESeq2 R package, and genes with significant changes in expression were identified as those with a p value <0.05 and a log2 (fold change) >2. Differentially expressed genes were subjected to enrichment analysis in KOBAS. An FDR value of 0.05 was used as a cut-off.

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PD-L1 Surface Expression Screening and Analysis: A high-throughput flow cytometry screening assay was established to identify metabolic molecules modulating inducible PD-L1 expression. BXPC3 cells were seeded in 96-well plates, stimulated with IFN-γ, and treated with candidate molecules. Oxitriptan's effect was confirmed by treating BXPC3, A549, and SKOV3 cells with various concentrations (e.g., 2 µM, 10 µM) of the compound for 24 or 48 hours, with or without IFN-γ stimulation. Cells were then harvested, stained with an anti-PD-L1 antibody, and analyzed by flow cytometry to quantify mean fluorescent intensity (MFI). [6]
Immunoblotting (Western Blot): To analyze protein expression, BXPC3, A549, and SKOV3 cells were treated with DMSO, IFN-γ, and/or Oxitriptan (10 µM) for various time points (1, 6, 12, 24 hours). Total cell lysates were separated on SDS-polyacrylamide gels, transferred to nitrocellulose membranes, and blotted with specific antibodies against PD-L1, ERK1/2, p-ERK1/2, c-JUN, p-c-JUN, and GAPDH. Protein bands were quantified using ImageJ. [6]
RNA Extraction and Quantitative Real-Time PCR (qPCR): To assess mRNA levels, BXPC3, A549, SKOV3, SW48, MC38, and CT26 cells were treated with IFN-γ and various concentrations of Oxitriptan for 24 or 48 hours. Total RNA was isolated, reverse transcribed to cDNA, and gene expression (PD-L1, RTK ligands) was detected by quantitative RT-PCR. GAPDH/Gapdh was used as an internal control, and fold changes were calculated using the ΔΔCt method. [6]
Small Interfering RNA (siRNA) Transfection: BXPC3 cells were plated in 12-well plates and transfected with siRNA targeting c-JUN using Lipofectamine RNAiMax according to the manufacturer's protocol. After transfection, cells were treated with IFN-γ and/or Oxitriptan (10 µM) for 24 hours, and PD-L1 mRNA expression was analyzed by qPCR to determine the role of c-JUN. [6]
Cytotoxicity Assay (MTT): MC38 and CT26 cells were seeded in 96-well plates and treated with Oxitriptan at concentrations of 10 µM, 50 µM, and 100 µM. After incubation, cell survival was determined by adding an MTT solution, and optical absorbance was measured to assess proliferation. [6]

Mice and in vivo tumor model [6]
Female 6–8 week-old C57BL/6 mice, BALB/c mice, and BALB/c nude mice were fed a standard laboratory diet and provided with free access to water. The animals were housed under standard laboratory conditions (21°C±2°C, 12-hour light–dark cycle). CT26 (3×105), MC38 (3×105/1×106), and MC38 Pd-l1−/− (1×106) cells were subcutaneously inoculated into BALB/c mice or C57BL/6 mice. L-5-HTP (dissolved in 5% DMSO in PBS) was injected intraperitoneally (100 mg/kg) once per day. PD-1 monoclonal antibody (150 µg dissolved in PBS) (Bio X cell) was administered intraperitoneally at day 8, 12, and 16 alone or combined with L-5-HTP. Body weight and tumor volume were measured every 3 days. Tumor volume was calculated as 1/2×(length×width2). Mice were sacrificed at the endpoint.

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Syngeneic Tumor Model:** Female 6-8 week-old C57BL/6 mice (for MC38) or BALB/c mice (for CT26) were subcutaneously inoculated with 3×10⁵ tumor cells. For the MC38 PD-L1 knockout experiment, 1×10⁶ MC38 wild-type or Pd-l1-/- cells were implanted. Oxitriptan was dissolved in 5% DMSO in PBS and administered via intraperitoneal injection at a dose of 100 mg/kg once daily, starting the day after tumor implantation. Tumor volume (calculated as 1/2 × (length × width²)) and body weight were measured every 3 days. At the endpoint, mice were sacrificed, and tumors were excised for further analysis (weight, IHC, flow cytometry). For survival studies, mice were monitored until a humane endpoint was reached. [6]
**Combination Therapy with PD-1 Antibody:** In the MC38 model, some groups received anti-PD-1 monoclonal antibody (150 µg in PBS) administered intraperitoneally on days 8, 12, and 16, either alone or in combination with daily Oxitriptan (100 mg/kg, i.p.). [6]
**Chronic Social Defeat Stress (CSDS)-Conditioned Tumor Model:** Mice were subjected to CSDS to induce depressive-like behaviors. Following this, tumor cells were implanted, and the effects of Oxitriptan on tumor growth and depression-related behaviors were assessed using the tail suspension test (TST) and sucrose preference test (SPT). [6]
**Intratumoral Immune Cell Analysis:** At the endpoint, tumors were excised, cut into small pieces, and digested with an enzyme cocktail (collagenase, hyaluronidase, DNase) for 60 minutes at 37°C. Cell suspensions were filtered and single immune cells were isolated using lymphocyte separation medium. Cells were then blocked, stained with surface and intracellular antibodies, and analyzed by flow cytometry. [6]
**Immunohistochemistry (IHC):** Tumor tissues were fixed in 4% paraformaldehyde, embedded in paraffin, and sectioned. Slides were stained with specific primary antibodies against PD-L1, CD8, and granzyme B, followed by appropriate secondary antibodies and hematoxylin counterstaining. Stained slides were scanned, and positively stained cells in random fields were quantified. [6]

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Syngeneic Tumor Model: Female 6-8 week-old C57BL/6 mice (for MC38) or BALB/c mice (for CT26) were subcutaneously inoculated with 3×10⁵ tumor cells. For the MC38 PD-L1 knockout experiment, 1×10⁶ MC38 wild-type or Pd-l1-/- cells were implanted. Oxitriptan was dissolved in 5% DMSO in PBS and administered via intraperitoneal injection at a dose of 100 mg/kg once daily, starting the day after tumor implantation. Tumor volume (calculated as 1/2 × (length × width²)) and body weight were measured every 3 days. At the endpoint, mice were sacrificed, and tumors were excised for further analysis (weight, IHC, flow cytometry). For survival studies, mice were monitored until a humane endpoint was reached. [6]
Combination Therapy with PD-1 Antibody: In the MC38 model, some groups received anti-PD-1 monoclonal antibody (150 µg in PBS) administered intraperitoneally on days 8, 12, and 16, either alone or in combination with daily Oxitriptan (100 mg/kg, i.p.). [6]
Chronic Social Defeat Stress (CSDS)-Conditioned Tumor Model: Mice were subjected to CSDS to induce depressive-like behaviors. Following this, tumor cells were implanted, and the effects of Oxitriptan on tumor growth and depression-related behaviors were assessed using the tail suspension test (TST) and sucrose preference test (SPT). [6]
Intratumoral Immune Cell Analysis: At the endpoint, tumors were excised, cut into small pieces, and digested with an enzyme cocktail (collagenase, hyaluronidase, DNase) for 60 minutes at 37°C. Cell suspensions were filtered and single immune cells were isolated using lymphocyte separation medium. Cells were then blocked, stained with surface and intracellular antibodies, and analyzed by flow cytometry. [6]
Immunohistochemistry (IHC): Tumor tissues were fixed in 4% paraformaldehyde, embedded in paraffin, and sectioned. Slides were stained with specific primary antibodies against PD-L1, CD8, and granzyme B, followed by appropriate secondary antibodies and hematoxylin counterstaining. Stained slides were scanned, and positively stained cells in random fields were quantified. [6]

Metabolism / Metabolites
5-Hydroxytryptophan is decarboxylated by aromatic L-amino acid decarboxylases in nerve tissue and liver via a vitamin B6-dependent reaction to generate serotonin (5-hydroxytryptophan or 5-HT).

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The concentration of Oxitriptan in tumor tissue and serum following intraperitoneal treatment at 100 mg/kg was determined by ultra-high-pressure liquid chromatography-mass spectrometry/mass spectrometry (UHPLC-MS/MS). Nearly 15 nmol/g of Oxitriptan (approximately 3 µg per mouse) was found in tumor tissues, and 14 µM was found in serum. [6]

The oral LD50 in rats was 243 mg/kg, with behavioral manifestations including lethargy (inhibition of overall activity), excitement, and ataxia. (Japanese Journal of Pharmacology, 69(523), 1973 [PMID:4546003]) The intraperitoneal LD50 in rats was 91 mg/kg, with behavioral manifestations including lethargy (inhibition of overall activity), excitement, and ataxia. (Japanese Journal of Pharmacology, 69(523), 1973) Japanese Journal of Pharmacology, 69(523), 1973 [PMID:4546003]
Subcutaneous LD50 in rats: 149 mg/kg. Sensory organs and special senses: tearing: eyes; behavior: tremor; behavior: convulsions or effect on epilepsy threshold. Medical Research, 6(307), 1975
Intravenous LD50 in rats: 27 mg/kg. Sensory organs and special senses: tearing: eyes; behavior: tremor; behavior: convulsions or effect on epilepsy threshold. Medical Research, 6(307), 1975
Oral LD50 in mice: 1708 mg/kg. Sensory organs and special senses: tearing; eyes; behavior: tremor; behavior: convulsions or effect on epilepsy threshold. Medical Research, 6(307), 1975

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In in vivo mouse tumor models (MC38 and CT26), daily intraperitoneal administration of Oxitriptan at 100 mg/kg was well tolerated, as no significant difference in body weight was detected between the vehicle-treated group and the Oxitriptan-treated group. In vitro, Oxitriptan at concentrations up to 100 µM did not have any significant deleterious effects on the proliferation of OVA-activated primary T cells isolated from OT-1 mice. [6]

[1]. 3,4-Dihydroxyphenylalanine and 5-Hydroxytryptophan as Reserpine Antagonists. Nature 180, page1200 (1957).

[2]. Double-blind study of 5-hydroxytryptophan versus placebo in the treatment of primary fibromyalgia syndrome. J Int Med Res. 1990 May-Jun;18(3):201-9.

[3]. Treatment of myoclonus with L-5-hydroxytryptophan and carbidopa: clinical, electrophysiological, and biochemical observations. Ann Neurol. 1980 Jun;7(6):570-6.

[4]. 5-OH-Tryptophane in migraine: clinical and neurophysiological considerations. J Neurol. 1981;225(1):41-6.

[5]. Improvement of cerebellar ataxia with levorotatory form of 5-hydroxytryptophan. A double-blind study with quantified data processing. Arch Neurol. 1988 Nov;45(11):1217-22.

[6]. L-5-hydroxytryptophan promotes antitumor immunity by inhibiting PD-L1 inducible expression. J Immunother Cancer. 2022 Jun;10(6):e003957.

L-5-Hydroxytryptophan is a colorless to pale pink crystal. (NTP, 1992)
5-Hydroxy-L-tryptophan is the L-enantiomer of 5-hydroxytryptophan. It is a human metabolite, a plant metabolite, and a mouse metabolite. It is a 5-hydroxytryptophan, hydroxy-L-tryptophan, and non-protein L-α-amino acid. It is an enantiomer of 5-hydroxy-D-tryptophan and also a zwitterion tautomer of 5-hydroxy-L-tryptophan.
5-Hydroxytryptophan (5-HTP), also known as oxitrazan (INN), is a naturally occurring amino acid and a metabolic intermediate in the synthesis of serotonin and melatonin. 5-HTP is available without a prescription as a dietary supplement in the UK, USA, and Canada for its antidepressant, appetite-suppressant, and sleep-aiding effects. In many European countries, 5-HTP is also marketed under brand names such as Cincofarm, Levothym, Levotonine, Oxyfan, Telesol, Tript-OH, and Triptum for the treatment of major depressive disorder. Multiple double-blind, placebo-controlled Khellinical trials have confirmed the effectiveness of 5-HTP in treating depression, but the lack of high-quality research is a concern. More research is needed to determine its efficacy in treating depression. 5-Hydroxy-L-tryptophan has been reported to be present in Aspergillus fumigatus, humans, and other organisms with relevant data. Osithraptan is an aromatic amino acid with antidepressant activity. In the body, oxithraptan (or 5-hydroxytryptophan) can be converted into serotonin (5-HT or serotonin) and other neurotransmitters. Osithraptan may exert its antidepressant effect by conversion to serotonin or by directly binding to serotonin (5-HT) receptors in the central nervous system (CNS). Endogenous oxithraptan is synthesized from the essential amino acid L-tryptophan. Exogenous therapeutic formulations are extracted from the seeds of the African plant Griffonia simplicifolia. 5-Hydroxytryptophan, DL-, is a racemic mixture of 5-hydroxytryptophan (5-HTP), a precursor to serotonin, a neurotransmitter with antidepressant, analgesic, and appetite-suppressing effects. DL-5-HTP is decarboxylated by aromatic L-amino acid decarboxylases to generate serotonin, leading to elevated serotonin levels in the brain. This elevated serotonin level, mediated by serotonin receptors, increases the transmission of the serotonin neurotransmitter, thereby alleviating depression, pain, and appetite. DL-5-HTP is a direct precursor to serotonin in the synthesis of tryptophan. It is used as an antiepileptic and antidepressant. See also: ... See more ...

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Drug Indications
Used as an antidepressant, appetite suppressant, and hypnotic agent.

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Pharmacodynamics
The psychoactive effects of 5-HTP are thought to be due to increased serotonin production in central nervous system tissues. Background: Inhibition or downregulation of programmed death-ligand 1 (PD-L1) can relieve its inhibitory effect on T cells and activate anti-tumor immune responses. Although PD-1 and PD-L1 antibodies are effective treatments for a variety of tumors, their inherent limitations and immune-related adverse events remain significant issues. The development of small molecule inhibitors targeting the interaction surfaces of PD-1 and PD-L1 is resurgent, but many challenges remain. To address these issues, we aimed to identify small molecules with durable efficacy and good biocompatibility that can alter PD-L1 surface expression and hold promise as alternatives to or complements to existing anti-PD-1/PD-L1 therapies. Methods: We used high-throughput flow cytometry to detect PD-L1 surface expression and performed a cell-based screening of 200 metabolic molecules, discovering that L-5-hydroxytryptophan (L-5-HTP) can inhibit interferon-γ (IFN-γ)-induced PD-L1 expression. We evaluated the inhibitory effect of L-5-HTP on PD-L1 induction and its antitumor activity in two homologous mouse tumor models. Furthermore, we investigated the changes in the tumor microenvironment induced by L-5-HTP treatment using flow cytometry. Results: We found that L-5-HTP can transcriptionally inhibit IFN-γ-induced PD-L1 expression in tumor cells, and this inhibition is a direct result of L-5-HTP itself. Mechanistically, L-5-HTP inhibits IFN-γ-induced RTK ligand expression, thereby suppressing RTK receptor phosphorylation activation and its downstream MEK/ERK/c-JUN signaling pathway, ultimately leading to reduced PD-L1 induction. In the homologous mouse tumor model, intraperitoneal injection of 100 mg/kg L-5-HTP inhibited PD-L1 expression and exerted an antitumor effect. L-5-HTP upregulated the proportion of granzyme B-positive CD8+ activated cytotoxic T cells. A intact immune system and PD-L1 expression are crucial for the antitumor effect of L-5-HTP. In addition, L-5-HTP has a synergistic effect with PD-1 antibodies, which can enhance the anti-cancer effect. Conclusion: Our study shows that L-5-HTP has an inhibitory effect on IFN-γ-stimulated PD-L1 induction in tumor cells, and provides a clue for using L-5-HTP for tumor immunotherapy. [6]

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Oxitriptan (L-5-HTP) is the precursor of serotonin (5-HT), an aromatic amino acid produced from L-tryptophan by tryptophan hydroxylase (TPH). It has been marketed as a nutritional supplement for treating depression for over 30 years. This study repurposes it for cancer immunotherapy, demonstrating its role in promoting antitumor immunity by inhibiting PD-L1 inducible expression. Oxitriptan acts synergistically with PD-1 antibody to improve anticancer effect. It also delayed tumor progression and relieved depression in a CSDS-conditioned tumor mouse model, suggesting potential benefits for cancer patients suffering from depression. [6]

220.084

C, 59.99; H, 5.49; N, 12.72; O, 21.80

4350-09-8

L-5-Hydroxytryptophan-d3;1276197-29-5;L-5-Hydroxytryptophan-d3-1;L-5-Hydroxytryptophan-d4;1246818-91-6

439280

White to light brown solid powder

1.5±0.1 g/cm3

520.6±50.0 °C at 760 mmHg

270 °C (dec.)(lit.)

268.7±30.1 °C

0.0±1.4 mmHg at 25°C

1.737

-0.14

4

4

3

16

272

1

O([H])C1C([H])=C([H])C2=C(C=1[H])C(=C([H])N2[H])C([H])([H])[C@@]([H])(C(=O)O[H])N([H])[H]

LDCYZAJDBXYCGN-VIFPVBQESA-N

InChI=1S/C11H12N2O3/c12-9(11(15)16)3-6-5-13-10-2-1-7(14)4-8(6)10/h1-2,4-5,9,13-14H,3,12H2,(H,15,16)/t9-/m0/s1

(2S)-2-amino-3-(5-hydroxy-1H-indol-3-yl)propanoic acid

5 Hydroxytryptophan; Oxitriptan; 5-hydroxy-L-tryptophan; L-5-Hydroxytryptophan; oxitriptan; 4350-09-8; Levothym; Cincofarm; Pretonine; L-5-Htp; 5-hydroxy-L-tryptophan; Oxytryptophan5-HTP

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~12.5 mg/mL (~56.76 mM)

Solubility in Formulation 1: ≥ 1.25 mg/mL (5.68 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 1.25 mg/mL (5.68 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)